A Cross-Sectional Study of Tobacco Advertising, Promotion, and Sponsorship in Airports across Europe and the United States

Altres ajuts: The work was supported by grant number 108594 from the Flight Attendant Medical Research Institute (FAMRI) to the Johns Hopkins FAMRI Center of Excellence. The funder had no role in the Int. J. Environ. Res. Public Health 2016, 13, 959 8 of 9 study design, collection, analysis or interpretation of data, writing of the report, nor in the decision to submit the paper for publication.Tobacco advertising, promotion, and sponsorship (TAPS) bans are effective and are increasingly being implemented in a number of venues and countries, yet the state of TAPS in airports and their effect on airport smoking behavior is unknown. The objective of this study was to evaluate the presence of TAPS in airports across Europe and the US, and to begin to examine the relationship between TAPS and smoking behaviors in airports. We used a cross-sectional study design to observe 21 airports in Europe (11) and the US (10). Data collectors observed points of sale for tobacco products, types of products sold, advertisements and promotions, and branding or logos that appeared in the airport. Tobacco products were sold in 95% of all airports, with significantly more sales in Europe than the US. Advertisements appeared mostly in post-security areas; however, airports with advertisements in pre-security areas had significantly more smokers observed outdoors than airports without advertisements in pre-security areas. Tobacco branding appeared in designated smoking rooms as well as on non-tobacco products in duty free shops. TAPS are widespread in airports in Europe and the US and might be associated with outdoor smoking, though further research is needed to better understand any relationship between the two. This study adds to a growing body of research on tobacco control in air transit and related issues. As smoke-free policies advance, they should include comprehensive TAPS bans that extend to airport facilities

Tropical cyclone exposure is associated with increased hospitalization rates in older adults

Hurricanes and other tropical cyclones have devastating effects on society. Previous case studies have quantified their impact on some health outcomes for particular tropical cyclones, but a comprehensive assessment over longer periods is currently missing. Here, we used data on 70 million Medicare hospitalizations and tropical cyclone exposures over 16 years (1999–2014). We formulated a conditional quasi-Poisson model to examine how tropical cyclone exposure (days greater than Beaufort scale gale-force wind speed; ≥34 knots) affect hospitalizations for 13 mutually-exclusive, clinically-meaningful causes. We found that tropical cyclone exposure was associated with average increases in hospitalizations from several causes over the week following exposure, including respiratory diseases (14.2%; 95% confidence interval [CI]: 10.9–17.9%); infectious and parasitic diseases (4.3%; 95%CI: 1.2–8.1%); and injuries (8.7%; 95%CI: 6.0–11.8%). Average decadal tropical cyclone exposure in all impacted counties would be associated with an estimated 16,772 (95%CI: 8,265–25,278) additional hospitalizations. Our findings demonstrate the need for targeted preparedness strategies for hospital personnel before, during, and after tropical cyclones

Arsenic Exposure and Hypertension: A Systematic Review

Background: Environmental exposure to arsenic has been linked to hypertension in persons living in arsenic-endemic areas

Arsenic Exposure and Type 2 Diabetes: A Systematic Review of the Experimental and Epidemiologic Evidence

Chronic arsenic exposure has been suggested to contribute to diabetes development. We performed a systematic review of the experimental and epidemiologic evidence on the association of arsenic and type 2 diabetes. We identified 19 in vitro studies of arsenic and glucose metabolism. Five studies reported that arsenic interfered with transcription factors involved in insulin-related gene expression: upstream factor 1 in pancreatic β-cells and peroxisome proliferative-activated receptor γ in preadipocytes. Other in vitro studies assessed the effect of arsenic on glucose uptake, typically using very high concentrations of arsenite or arsenate. These studies provide limited insight on potential mechanisms. We identified 10 in vivo studies in animals. These studies showed inconsistent effects of arsenic on glucose metabolism. Finally, we identified 19 epidemiologic studies (6 in high-arsenic areas in Taiwan and Bangladesh, 9 in occupational populations, and 4 in other populations). In studies from Taiwan and Bangladesh, the pooled relative risk estimate for diabetes comparing extreme arsenic exposure categories was 2.52 (95% confidence interval, 1.69–3.75), although methodologic problems limit the interpretation of the association. The evidence from occupational studies and from general populations other than Taiwan or Bangladesh was inconsistent. In summary, the current available evidence is inadequate to establish a causal role of arsenic in diabetes. Because arsenic exposure is widespread and diabetes prevalence is reaching epidemic proportions, experimental studies using arsenic concentrations relevant to human exposure and prospective epidemiologic studies measuring arsenic biomarkers and appropriately assessing diabetes should be a research priority

Analysis of urinary potassium isotopes and association with pancreatic health: healthy, diabetic and cancerous states

Background: More than 700 million people worldwide suffer from diseases of the pancreas, such as diabetes, pancreatitis and pancreatic cancer. Often dysregulation of potassium (K+) channels, co-transporters and pumps can promote development and progression of many types of these diseases. The role of K+ transport system in pancreatic cell homeostasis and disease development remains largely unexplored. Potassium isotope analysis (δ41K), however, might have the potential to detect minute changes in metabolic processes relevant for pancreatic diseases. Methods: We assessed urinary K isotope composition in a case-control study by measuring K concentrations and δ41K in spot urines collected from patients diagnosed with pancreatic cancer (n=18), other pancreas-related diseases (n=14) and compared those data to healthy controls (n=16). Results: Our results show that urinary K+ levels for patients with diseased pancreas (benign and pancreatic cancer) are significantly lower than the healthy controls. For δ41K, the values tend to be higher for individuals with pancreatic cancer (mean δ41K = -0.58 ± 0.33‰) than for healthy individuals (mean δ41K = -0.78 ± 0.19‰) but the difference is not significant (p=0.08). For diabetics, urinary K+ levels are significantly lower (p=0.03) and δ41K is significantly higher (p=0.009) than for the healthy controls. These results suggest that urinary K+ levels and K isotopes can help identify K disturbances related to diabetes, an associated factors of all-cause mortality for diabetics. Conclusion: Although the K isotope results should be considered exploratory and hypothesis-generating and future studies should focus on larger sample size and δ41K analysis of other K-disrupting diseases (e.g., chronic kidney disease), our data hold great promise for K isotopes as disease marker

A preliminary assessment of low level arsenic exposure and diabetes mellitus in Cyprus

<p>Abstract</p> <p>Background</p> <p>A preliminary study was undertaken in a community of Cyprus where low-level arsenic (As) concentrations were recently detected in the groundwater that was chronically used to satisfy potable needs of the community. The main objective of the study was to assess the degree of association between orally-ingested As and self-reported type-2 diabetes mellitus (DM) in 317 adult (≥18 years old) volunteers.</p> <p>Methods</p> <p>Cumulative lifetime As exposure (CLAEX) (mg As) was calculated using the median As concentrations in water, individual reported daily water consumption rates, and lifetime exposure duration. Logistic regression models were used to model the probability of self-reported DM and calculate odds ratios (OR) in univariate and multivariate models.</p> <p>Results</p> <p>Significantly higher (p <it><</it> 0.02) CLAEX values were reported for the diabetics (median = 999 mg As) versus non-diabetics (median = 573 mg As), suggesting that As exposure could perhaps be related to the prevalence of DM in the study area, which was 6.6%. The OR for DM, comparing participants in the 80^th versus the 20^th percentiles of low-level As CLAEX index values, was 5.0 (1.03, 24.17), but after adjusting for age, sex, smoking, education, and fish consumption, the As exposure effect on DM was not significant.</p> <p>Conclusions</p> <p>Further research is needed to improve As exposure assessment for the entire Cypriot population while assessing the exact relationship between low-level As exposure and DM.</p

Association of single and joint metals with albuminuria and estimated glomerular filtration longitudinal change in middle-aged adults from Spain: The Aragon workers health study

The nephrotoxicity of low-chronic metal exposures is unclear, especially considering several metals simultaneously. We assessed the individual and joint association of metals with longitudinal change in renal endpoints in Aragon Workers Health Study participants with available measures of essential (cobalt [Co], copper [Cu], molybdenum [Mo] and zinc [Zn]) and non-essential (As, barium [Ba], Cd, chromium [Cr], antimony [Sb], titanium [Ti], uranium [U], vanadium [V] and tungsten [W]) urine metals and albumin-to-creatinine ratio (ACR) (N = 707) and estimated glomerular filtration rate (eGFR) (N = 1493) change. Median levels were 0.24, 7.0, 18.6, 295, 3.1, 1.9, 0.28, 1.16, 9.7, 0.66, 0.22 μg/g for Co, Cu, Mo, Zn, As, Ba, Cd, Cr, Sb, Ti, V and W, respectively, and 52.5 and 27.2 ng/g for Sb and U, respectively. In single metal analysis, higher As, Cr and W concentrations were associated with increasing ACR annual change. Higher Zn, As and Cr concentrations were associated with decreasing eGFR annual change. The shape of the longitudinal dose-responses, however, was compatible with a nephrotoxic role for all metals, both in ACR and eGFR models. In joint metal analysis, both higher mixtures of Cu–Zn–As–Ba–Ti–U–V–W and Co–Cd–Cr–Sb–V–W showed associations with increasing ACR and decreasing eGFR annual change. As and Cr were main drivers of the ACR change joint metal association. For the eGFR change joint metal association, while Zn and Cr were main drivers, other metals also contributed substantially. We identified potential interactions for As, Zn and W by other metals with ACR change, but not with eGFR change. Our findings support that Zn, As, Cr and W and suggestively other metals, are nephrotoxic at relatively low exposure levels. Metal exposure reduction and mitigation interventions may improve prevention and decrease the burden of renal disease in the population

Blood DNA methylation and liver cancer in American Indians: evidence from the Strong Heart Study

Purpose: Liver cancer incidence among American Indians/Alaska Natives has risen over the past 20 years. Peripheral blood DNA methylation may be associated with liver cancer and could be used as a biomarker for cancer risk. We evaluated the association of blood DNA methylation with risk of liver cancer. Methods: We conducted a prospective cohort study in 2324 American Indians, between age 45 and 75 years, from Arizona, Oklahoma, North Dakota and South Dakota who participated in the Strong Heart Study between 1989 and 1991. Liver cancer deaths (n = 21) were ascertained using death certificates obtained through 2017. The mean follow-up duration (SD) for non-cases was 25.1 (5.6) years and for cases, 11.0 (8.8) years. DNA methylation was assessed from blood samples collected at baseline using MethylationEPIC BeadChip 850 K arrays. We used Cox regression models adjusted for age, sex, center, body mass index, low-density lipoprotein cholesterol, smoking, alcohol consumption, and immune cell proportions to examine the associations. Results: We identified 9 CpG sites associated with liver cancer. cg16057201 annotated to MRFAP1) was hypermethylated among cases vs. non-cases (hazard ratio (HR) for one standard deviation increase in methylation was 1.25 (95% CI 1.14, 1.37). The other eight CpGs were hypomethylated and the corresponding HRs (95% CI) ranged from 0.58 (0.44, 0.75) for cg04967787 (annotated to PPRC1) to 0.77 (0.67, 0.88) for cg08550308. We also assessed 7 differentially methylated CpG sites associated with liver cancer in previous studies. The adjusted HR for cg15079934 (annotated to LPS1) was 1.93 (95% CI 1.10, 3.39). Conclusions: Blood DNA methylation may be associated with liver cancer mortality and may be altered during the development of liver cancer.This work was supported by grants from the National Heart, Lung, and Blood Institute (NHLBI) (Contract Numbers 75N92019D00027, 75N92019D00028, 75N92019D00029 and 75N92019D00030) and previous Grants (R01HL090863, R01HL109315, R01HL109301, R01HL109284, R01HL109282, and R01HL109319 and Cooperative Agreements: U01HL41642, U01HL41652, U01HL41654, U01HL65520 and U01HL65521); by the National Institute of Environmental Health Sciences (Grant Numbers R25ES025505, R01ES032638, R01ES021367, R01ES025216, P42ES033719, P30ES009089); by the Chilean CONICYT/FONDECYT-POSTDOCTORADO Nº 3180486 and by a fellowship from “la Caixa” Foundation (ID 100010434) (fellowship code “LCF/BQ/DR19/11740016”). The funders had no role in the planning, conducting, analysis, interpretation, or writing of this study. The content of this manuscript is solely the responsibility of the authors and does not necessarily represent the ofcial views of the National Institutes of Health (United States) or the National Health Institute Carlos III (Spain).S

Blood DNA methylation and liver cancer in American Indians: evidence from the strong heart study

Liver cancer incidence among American Indians/Alaska Natives has risen over the past 20 years. Peripheral blood DNA methylation may be associated with liver cancer and could be used as a biomarker for cancer risk. We evaluated the association of blood DNA methylation with risk of liver cancer. We conducted a prospective cohort study in 2324 American Indians, between age 45 and 75 years, from Arizona, Oklahoma, North Dakota and South Dakota who participated in the Strong Heart Study between 1989 and 1991. Liver cancer deaths (n = 21) were ascertained using death certificates obtained through 2017. The mean follow-up duration (SD) for non-cases was 25.1 (5.6) years and for cases, 11.0 (8.8) years. DNA methylation was assessed from blood samples collected at baseline using MethylationEPIC BeadChip 850 K arrays. We used Cox regression models adjusted for age, sex, center, body mass index, low-density lipoprotein cholesterol, smoking, alcohol consumption, and immune cell proportions to examine the associations. We identified 9 CpG sites associated with liver cancer. cg16057201 annotated to MRFAP1) was hypermethylated among cases vs. non-cases (hazard ratio (HR) for one standard deviation increase in methylation was 1.25 (95% CI 1.14, 1.37). The other eight CpGs were hypomethylated and the corresponding HRs (95% CI) ranged from 0.58 (0.44, 0.75) for cg04967787 (annotated to PPRC1) to 0.77 (0.67, 0.88) for cg08550308. We also assessed 7 differentially methylated CpG sites associated with liver cancer in previous studies. The adjusted HR for cg15079934 (annotated to LPS1) was 1.93 (95% CI 1.10, 3.39). Blood DNA methylation may be associated with liver cancer mortality and may be altered during the development of liver cancerThis work was supported by grants from the National Heart, Lung, and Blood Institute (NHLBI) (Contract Numbers 75N92019D00027, 75N92019D00028, 75N92019D00029 and 75N92019D00030) and previous Grants (R01HL090863, R01HL109315, R01HL109301, R01HL109284, R01HL109282, and R01HL109319 and Cooperative Agreements: U01HL41642, U01HL41652, U01HL41654, U01HL65520 and U01HL65521); by the National Institute of Environmental Health Sciences (Grant Numbers R25ES025505, R01ES032638, R01ES021367, R01ES025216, P42ES033719, P30ES009089); by the Chilean CONICYT/FONDECYT-POSTDOCTORADO Nº 3180486 and by a fellowship from “la Caixa” Foundation (ID 100010434) (fellowship code “LCF/BQ/DR19/11740016”). The funders had no role in the planning, conducting, analysis, interpretation, or writing of this study. The content of this manuscript is solely the responsibility of the authors and does not necessarily represent the ofcial views of the National Institutes of Health (United States) or the National Health Institute Carlos III (Spain

Genetic variation and urine cadmium levels: ABCC1 effects in the Strong Heart Family Study

Genetic effects are suspected to influence cadmium internal dose. Our objective was to assess genetic determinants of urine cadmium in American Indian adults participating in the Strong Heart Family Study (SHFS). Urine cadmium levels and genotyped short tandem repeat (STR) markers were available on 1936 SHFS participants. We investigated heritability, including gene-by-sex and smoking interactions, and STR-based quantitative trait locus (QTL) linkage, using a variance-component decomposition approach, which incorporates the genetic information contained in the pedigrees. We also used available single nucleotide polymorphisms (SNPs) from Illumina's Metabochip and custom panel to assess whether promising QTLs associated regions could be attributed to SNPs annotated to specific genes. Median urine cadmium levels were 0.44 μg/g creatinine. The heritability of urine cadmium concentrations was 28%, with no evidence of gene-by-sex or -smoking interaction. We found strong statistical evidence for a genetic locus at chromosome 16 determining urine cadmium concentrations (Logarithm of odds score [LOD] = 3.8). Among the top 20 associated SNPs in this locus, 17 were annotated to ABCC1 (p-values from 0.0002 to 0.02), and attenuated the maximum linkage peak by a ∼40%. Suggestive QTL signals (LOD>1.9) in chromosomes 2, 6, 11, 14, and 19, showed associated SNPs in the genes NDUFA10, PDE10A, PLEKHA7, BAZ1A and CHAF1A, respectively. Our findings support that urinary cadmium levels are heritable and influenced by a QTL on chromosome 16, which was explained by genetic variation in ABCC1. Studies with extended sets of genome-wide markers are needed to confirm these findings and to identify additional metabolism and toxicity pathways for cadmium