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BACKGROUND: Urinary cadmium (U-Cd) has been associated with decreased peripheral bone mineral density (BMD) and osteoporosis. This association, however, has not been confirmed using femoral BMD, the international standard for [...]

BACKGROUND: Chronic diseases, including coronary heart disease (CHD), have been associated with ingestion of drinking water with high levels of inorganic arsenic (> 1,000 [micro]g/L). However, associations have been inconclusive in populations with lower levels (< 100 [micro]g/L) of inorganic arsenic exposure. OBJECTIVES: We conducted a case-cohort study based on individual estimates of lifetime arsenic exposure to examine the relationship between chronic low-level arsenic exposure and risk of CHD. METHODS: This study included 555 participants with 96 CHD events diagnosed between 1984 and 1998 for which individual lifetime arsenic exposure estimates were determined using data from structured interviews and secondary data sources to determine lifetime residence, which was linked to a geospatial model of arsenic concentrations in drinking water. These lifetime arsenic exposure estimates were correlated with historically collected urinary arsenic concentrations. A Cox proportional-hazards model with time-dependent CHD risk factors was used to assess the association between time-weighted average (TWA) lifetime exposure to low-level inorganic arsenic in drinking water and incident CHD. RESULTS: We estimated a positive association between low-level inorganic arsenic exposure and CHD risk [hazard ratio (HR): = 1.38, 95% CI: 1.09, 1.78] per 15 [micro]g/L while adjusting for age, sex, first-degree family history of CHD, and serum low-density lipoprotein levels. The risk of CHD increased monotonically with increasing TWAs for inorganic arsenic exposure in water relative to < 20 [micro]g/L (HR = 1.2, 95% CI: 0.6, 2.2 for 20-30 [micro]g/L; HR = 2.2; 95% CI: 1.2, 4.0 for 30-45 [micro]g/L; and HR = 3, 95% CI: 1.1, 9.1 for 45-88 [micro]g/L). CONCLUSIONS: Lifetime exposure to low-level inorganic arsenic in drinking water was associated with increased risk for CHD in this population. citation: James KA, Byers T, Hokanson JE, Meliker JR, Zerbe GO, Marshall JA. 2015. Association between lifetime exposure to inorganic arsenic in drinking water and coronary heart disease in Colorado residents. Environ Health Perspect 123:128-134; http://dx.doi.org/10.1289/ehp.1307839, Introduction Nonoccupational exposure to inorganic arsenic occurs mainly through drinking contaminated water [U.S. Environmental Protection Agency (EPA) 1988]. In recent decades, research has identified a relationship between exposure to high [...]

Abstract Background Ingestion of groundwater with high concentrations of inorganic arsenic has been linked to adverse health outcomes, including bladder cancer, however studies have not consistently observed any elevation in risk at lower concentrations. Genetic variability in the metabolism and clearance of arsenic is an important consideration in any investigation of its potential health risks. Therefore, we examined the association between genes thought to play a role in the metabolism of arsenic and bladder cancer. Methods Single nucleotide polymorphisms (SNPs) in GSTO-1, As3MT and MTHFR were genotyped using DNA from 219 bladder cancer cases and 273 controls participating in a case–control study in Southeastern Michigan and exposed to low to moderate ( Results While no single SNP in As3MT was significantly associated with bladder cancer overall, several SNPs were associated with bladder cancer among those exposed to higher arsenic levels. Individuals with one or more copies of the C allele in rs11191439 (the Met287Thr polymorphism) had an elevated risk of bladder cancer (OR = 1.17; 95% CI = 1.04-1.32 per 1 μg/L increase in average exposure). However, no association was observed between average arsenic exposure and bladder cancer among TT homozygotes in the same SNP. Bladder cancer cases were also 60% less likely to be homozygotes for the A allele in rs1476413 in MTHFR compared to controls (OR = 0.40; 95% CI = 0.18-0.88). Conclusions Variation in As3MT and MTHFR is associated with bladder cancer among those exposed to relatively low concentrations of inorganic arsenic. Further investigation is warranted to confirm these findings.

BACKGROUND: In vitro and animal data suggest that cadmium, a heavy metal that contaminates some foods and tobacco plants, is an estrogenic endocrine disruptor. Elevated estrogen exposure is associated with breast, endometrial, and ovarian cancer risk. OBJECTIVES: We examined the association between dietary cadmium intake and risk of these cancers in the large, well-characterized Women's Health Initiative (WHI). METHODS: A total of 155,069 postmenopausal women, 50-79 years of age, who were enrolled in the WHI clinical trials or observational study, participated in this study. We estimated dietary cadmium consumption by combining baseline food frequency questionnaire responses with U.S. Food and Drug Administration data on food cadmium content. Participants reported incident invasive breast, endometrial, or ovarian cancer, and WHI centrally adjudicated all cases through August 2009. We applied Cox regression to estimate adjusted hazard ratios (HRs) and 95% CIs for each cancer, comparing quintiles of energy-adjusted dietary cadmium intake. RESULTS: Over an average of 10.5 years, 6,658 invasive breast cancers, 1,198 endometrial cancers, and 735 ovarian cancers were reported. We observed no statistically significant associations between dietary cadmium and risk of any of these cancers after adjustment for potential confounders including total dietary energy intake. Results did not differ in any subgroup of women examined. CONCLUSIONS: We found little evidence that dietary cadmium is a risk factor for breast, endometrial, or ovarian cancers in postmenopausal women. Misclassification in dietary cadmium assessment may have attenuated observed associations. http://dx.doi.org/10.1289/ehp.1307054, Introduction Cadmium, a carcinogenic heavy metal, is released into the environment as a result of industrial and agricultural activities (Jarup and Akesson 2009). Tobacco, grains, and some vegetables can take [...]

Abstract Background Our progress towards the goal of eliminating racial health disparities requires methods for assessing the existence, magnitude, and statistical significance of health disparities. In comparing disease rates, we must account for the unreliability of rates computed for small minority populations and within sparsely populated areas. Furthermore, as the number of geographic units under study increases, we also must account for multiple testing to assure we do not misclassify disparities as present when they actually are not (false positive). To date and to our knowledge, none of the methodologies in current use simultaneously address all of these important needs. And few, if any studies have undertaken a systematic comparison of methods to identify those that are statistically robust and reliable. Results We introduced six test statistics for quantifying absolute and relative differences between cancer rates measured in distinct groups (i.e. race or ethnicity). These alternative measures were illustrated using age-adjusted prostate and lung cancer mortality rates for white and black males in 688 counties of the Southeastern US (1970–1994). Statistical performance, including power and proportion of false positives, was investigated in simulation studies that mimic different scenarios for the magnitude and frequency of disparities. Two test statistics, which are based on the difference and ratio of rates, consistently outperformed the other measures. Corrections for multiple testing actually increased misclassification compared with the unadjusted tests and are not recommended. One-tailed tests allowed the researcher to consider a priori hypotheses beyond the basic test that the two rates are different. Conclusion The assessment of significant racial disparities across geographic areas is an important tool in guiding cancer control practices, and public health officials must consider the problems of small population size and multiple comparison, and should conduct disparity analyses using both absolute (difference, RD statistic) and relative (ratio, RR statistic) measures. Simple test statistics to assess the significance of rate difference and rate ratio perform well, and their unadjusted p-values provide a realistic assessment of the proportion of type I errors (i.e. disparities wrongly declared significant).

Abstract Background Exposure to arsenic concentrations in drinking water in excess of 300 μg/L is associated with diseases of the circulatory and respiratory system, several types of cancer, and diabetes; however, little is known about the health consequences of exposure to low-to-moderate levels of arsenic (10–100 μg/L). Methods A standardized mortality ratio (SMR) analysis was conducted in a contiguous six county study area of southeastern Michigan to investigate the relationship between moderate arsenic levels and twenty-three selected disease outcomes. Disease outcomes included several types of cancer, diseases of the circulatory and respiratory system, diabetes mellitus, and kidney and liver diseases. Arsenic data were compiled from 9251 well water samples tested by the Michigan Department of Environmental Quality from 1983 through 2002. Michigan Resident Death Files data were amassed for 1979 through 1997 and sex-specific SMR analyses were conducted with indirect adjustment for age and race; 99% confidence intervals (CI) were reported. Results The six county study area had a population-weighted mean arsenic concentration of 11.00 μg/L and a population-weighted median of 7.58 μg/L. SMR analyses were conducted for the entire six county study area, for only Genesee County (the most populous and urban county), and for the five counties besides Genesee. Concordance of results across analyses is used to interpret the findings. Elevated mortality rates were observed for both males (M) and females (F) for all diseases of the circulatory system (M SMR, 1.11; CI, 1.09–1.13; F SMR, 1.15; CI, 1.13,-1.17), cerebrovascular diseases (M SMR, 1.19; CI, 1.14–1.25; F SMR, 1.19; CI, 1.15–1.23), diabetes mellitus (M SMR, 1.28; CI, 1.18–1.37; F SMR, 1.27; CI, 1.19–1.35), and kidney diseases (M SMR, 1.28; CI, 1.15–1.42; F SMR, 1.38; CI, 1.25–1.52). Conclusion This is some of the first evidence to suggest that exposure to low-to-moderate levels of arsenic in drinking water may be associated with several of the leading causes of mortality, although further epidemiologic studies are required to confirm the results suggested by this ecologic SMR analysis.

Abstract Background Methods for analyzing space-time variation in risk in case-control studies typically ignore residential mobility. We develop an approach for analyzing case-control data for mobile individuals and apply it to study bladder cancer in 11 counties in southeastern Michigan. At this time data collection is incomplete and no inferences should be drawn – we analyze these data to demonstrate the novel methods. Global, local and focused clustering of residential histories for 219 cases and 437 controls is quantified using time-dependent nearest neighbor relationships. Business address histories for 268 industries that release known or suspected bladder cancer carcinogens are analyzed. A logistic model accounting for smoking, gender, age, race and education specifies the probability of being a case, and is incorporated into the cluster randomization procedures. Sensitivity of clustering to definition of the proximity metric is assessed for 1 to 75 k nearest neighbors. Results Global clustering is partly explained by the covariates but remains statistically significant at 12 of the 14 levels of k considered. After accounting for the covariates 26 Local clusters are found in Lapeer, Ingham, Oakland and Jackson counties, with the clusters in Ingham and Oakland counties appearing in 1950 and persisting to the present. Statistically significant focused clusters are found about the business address histories of 22 industries located in Oakland (19 clusters), Ingham (2) and Jackson (1) counties. Clusters in central and southeastern Oakland County appear in the 1930's and persist to the present day. Conclusion These methods provide a systematic approach for evaluating a series of increasingly realistic alternative hypotheses regarding the sources of excess risk. So long as selection of cases and controls is population-based and not geographically biased, these tools can provide insights into geographic risk factors that were not specifically assessed in the case-control study design.

Abstract Background Recent years have seen an expansion in the use of Geographic Information Systems (GIS) in environmental health research. In this field GIS can be used to detect disease clustering, to analyze access to hospital emergency care, to predict environmental outbreaks, and to estimate exposure to toxic compounds. Despite these advances the inability of GIS to properly handle temporal information is increasingly recognised as a significant constraint. The effective representation and visualization of both spatial and temporal dimensions therefore is expected to significantly enhance our ability to undertake environmental health research using time-referenced geospatial data. Especially for diseases with long latency periods (such as cancer) the ability to represent, quantify and model individual exposure through time is a critical component of risk estimation. In response to this need a STIS – a Space Time Information System has been developed to visualize and analyze objects simultaneously through space and time. Results In this paper we present a "first use" of a STIS in a case-control study of the relationship between arsenic exposure and bladder cancer in south eastern Michigan. Individual arsenic exposure is reconstructed by incorporating spatiotemporal data including residential mobility and drinking water habits. The unique contribution of the STIS is its ability to visualize and analyze residential histories over different temporal scales. Participant information is viewed and statistically analyzed using dynamic views in which values of an attribute change through time. These views include tables, graphs (such as histograms and scatterplots), and maps. In addition, these views can be linked and synchronized for complex data exploration using cartographic brushing, statistical brushing, and animation. Conclusion The STIS provides new and powerful ways to visualize and analyze how individual exposure and associated environmental variables change through time. We expect to see innovative space-time methods being utilized in future environmental health research now that the successful "first use" of a STIS in exposure reconstruction has been accomplished.

Ionizing radiation at diagnostic and therapeutic doses is a known contributor to the development of brain and spinal cord (CNS) cancer. However, little is known about risk from exposure to radon, a natural radiation source which the general population is exposed to residentially and environmentally. This study investigated correlations between mean county radon levels and CNS cancer incidence in five highly populated and radon-enriched US states (Minnesota, mean radon level 4.6 pCi/L; Wisconsin, 5.7 pCi/L; Pennsylvania, 8.6 pCi/L; Iowa, 6.1 pCi/L; and New Jersey, 4.4 pCi/L). Mean radon levels per county were accessed through AirChek, which provides publicly available radon data measured in residences and workplaces. CNS cancer incidence data were accessed through the states' health department websites and span differing amounts of time due to the publicly accessible nature of the data, though all time spans were over 10 years. Negative binomial regressions were run to assess correlations between mean radon and CNS cancer incidence per county. Quantile maps were constructed and Moran's I was calculated to assess spatial autocorrelation in residuals; no spatial autocorrelation was evident. Iowa was the only state with a significant positive association between radon and CNS incidence; no associations were detected in other states, and a negative association was observed in the 5 states combined. This study does not provide evidence that radon is a risk factor for CNS cancer; however, the possibility of an association cannot be ruled out due to limitations of the study, principally its ecologic nature and lack of individual-level exposure data. [ABSTRACT FROM AUTHOR]

Exposure to lead (Pb) is implicated in a plethora of health threats in both adults and children. Increased exposure levels are associated with oxidative stress in the blood of workers exposed at occupational levels. However, it is not known whether lower Pb exposure levels are related to a shift toward a more oxidized state. To assess the association between blood lead level (BLL) and glutathione (GSH) redox biomarkers in a population of healthy adults, BLL and four GSH markers (GSH, GSSG, GSH/GSSG ratio and redox potential Eh) were measured in the blood of a cross-sectional cohort of 282 avid seafood-eating healthy adults living on Long Island (NY). Additionally, blood levels of two other metals known to affect GSH redox status, selenium (Se) and mercury (Hg), and omega-3 index were tested for effect modification. Regression models were further adjusted for demographic and smoking status. Increasing exposure to Pb, measured in blood, was not associated with GSSG, but was associated with lower levels of GSH/GSSG ratio and more positive GSH redox potential Eh, driven by its association with GSH. No effect modification was observed in analyses stratified by Hg, Se, omega-3 index, sex, age, or smoking. Blood Pb is associated with lower levels of GSH and the GSH/GSSG ratio in this cross-sectional study of healthy adults. [ABSTRACT FROM AUTHOR]

Mercury (Hg), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) concentrations differ across seafood types. Our aim was to investigate the association of Hg, EPA, and DHA, as well as avid consumption of diverse seafood types, with cardiovascular variables heart rate variability (HRV) and QT interval duration (QTc) in a contemporary population. We measured HRV and QTc by Holter monitor, EPA and DHA in plasma, total Hg in whole blood, and possible confounders in 94 avid seafood consumers from Long Island, NY. Participants had mean Hg of 8.4 mcg/L, mean EPA of 1.2%, and mean DHA of 3.7% of total fatty acids. Adjusted for possible confounders, EPA+DHA, Hg, and total seafood consumption were not associated with HRV or QTc. Associations with consumption of specific seafood types were suggested (eg, tuna steak with QTc and anchovies with HRV) but require verification. [ABSTRACT FROM AUTHOR]

Background: Few studies have investigated the association between radon and thyroid cancer despite the sensitivity of the thyroid gland to radiation. Our goal is to investigate the association between county-level radon and incidence of female thyroid cancer in the US States of Iowa, New Jersey, and Wisconsin. Methods: Thyroid cancer incidence data were provided by individual state cancer registries and span 1990-2013. Radon data come from a publicly available third-party database, AirChek, accessed in 2017. We tabulated the percent of radon above four picocuries per liter and the female thyroid cancer incidence rate in each county. Quantile maps were constructed, and an ordinary least-squares regression model was run using Geoda 1.10.0.8 (Chicago, IL, USA). Results: No association was observed between county-level radon and incidence of female thyroid cancer in any of the States: New Jersey (β = 0.06, p = 0.23); Iowa (β = -0.07, p = 0.07); orWisconsin (β = -0.01, p = 0.78). A spatial regression model was considered, but the Moran's I of the residuals from each of the models was not significant, so no spatial term was required. Discussion: In this county-level ecological study across three different States in the US, we did not find an association between elevated radon and thyroid cancer incidence in women. While this ecologic study reports null findings, due to the ecologic fallacy, individual-level studies of this association may still be warranted. [ABSTRACT FROM AUTHOR]