Does arsenic exposure increase the risk for diabetes mellitus?

OBJECTIVE: Long-term arsenic exposure has been reported to associated with prevalence, incidence, and mortality of diabetes mellitus (DM). A tap water supply system was implemented in the early 1960s in the blackfoot disease (BFD) endemic areas. The objective of this study is to examine whether DM mortality decreased after the improvement of drinking water supply system through elimination of arsenic exposure from artesian well water. METHODS: Standardized mortality ratios (SMRs) for DM were calculated for the BFD endemic area for the years 1971-2000. RESULTS: The study results show that mortality from DM declined in females (but not in males) gradually after the improvement of drinking water supply system. CONCLUSIONS: Based on the reversibility criterion, the association between arsenic exposure and DM is likely to be casual for females but not in males.     

Does arsenic exposure increase the risk for circulatory disease?

Studies of residents in communities with high endemic concentrations of arsenic in drinking water suggest a deleterious effect on the circulatory system; however, studies among workers with high occupational exposures generally have shown either no or weak associations. This discrepancy could be a result of the healthy worker effect, including the healthy hire component and the healthy worker survivor effect (HWSE). Therefore, the authors conducted analyses of arsenic exposure in relation to circulatory disease mortality among 2,802 Tacoma, Washington, smelter workers by using 1) internal comparisons to control for the healthy hire effect and 2) the lagging method, adjustment for employment status, and the G-null test to control for the HWSE. Both lagging and adjustment for work status increased circulatory mortality rate ratios at all exposure levels, as compared with a baseline Poisson model. This excess mortality was limited to cardiovascular disease; no excess was observed for cerebrovascular disease. G-null analyses suggested no adverse effect, but power was very limited for this analysis. Overall, these results may indicate that the HWSE obscures an effect of arsenic on circulatory disease. Since cardiovascular deaths constitute about one-third of total mortality, small rate ratios translate into large numbers of excess deaths and, if causal, could be of wide public health significance. Further studies of arsenic exposure and cardiovascular disease are needed, and those conducted in occupational cohorts must control for the HWSE.     

Does alcohol increase the risk of preterm delivery?

We evaluated the association between alcohol intake during pregnancy and preterm delivery. Women attending routine antenatal care at Aarhus University Hospital, Denmark, from 1989-1991 and 1992-1996 were eligible. We included 18,228 singleton pregnancies in the analyses. We obtained prospective information on alcohol intake at 16 and 30 weeks of gestation, other lifestyle factors, maternal characteristics, and obstetrical risk factors from self-administered questionnaires and hospital files. For women with alcohol intake of 1-2, 3-4, 5-9, and > or =10 drinks/week the risk ratio (RR) of preterm delivery was 0.91 (95% CI = 0.76-1.08), 0.86 (95% CI = 0.64-1.15), 0.89 (95% CI = 0.52-1.52), and 2.93 (95% CI = 1.52-5.63), respectively, compared with intake of <1 drink/week at 16 weeks gestation, and 0.69 (95% CI = 0.56-0.86), 0.82 (95% CI = 0.60-1.13), 0.97 (95% CI = 0.58-1.64), and 3.56 (95% CI = 1.78-7.13) at 30 weeks. Adjustment for smoking habits, caffeine intake, age, height, pre-pregnant weight, marital status, occupational status, education, parity, chronic diseases, previous preterm delivery, mode of initiation of labor, and sex of the child did not change the conclusions, nor did restriction of the highest intake group to women drinking 10-14 drinks/week (RR = 3.41 (1.71-6.81) at 16 weeks and RR = 3.47 (1.64-7.35) at 30 weeks).     

Does depression increase the risk of developing type 2 diabetes?

BACKGROUND: Members of a scheme awarding injury pensions may allege that the onset of diabetes was precipitated or caused by depression induced by work in order to claim an injury award. AIMS: To quantify the association between depression and subsequent development of type 2 diabetes in order to determine whether an individual in a pension scheme that awards injury pensions, who develops type 2 diabetes, should be awarded an injury pension, if the development of the diabetes followed a work-related depressive episode. METHODS: Electronic and hand literature searches up to December 2006. Relative risk estimates from cohort studies of adults were pooled using fixed and random effects models. Attributable risk fraction was calculated using the Levin formula. RESULTS: The presence of depression or depressive symptoms was associated with increased risk of subsequently developing type 2 diabetes. The pooled fully adjusted relative risk estimate from the three highest quality studies was 1.25 (95% CI: 1.02-1.48) and was homogenous. However, depression was no more frequent among those with and without prevalent, but previously undiagnosed, type 2 diabetes. CONCLUSION: Depression is associated with subsequent development of type 2 diabetes. However, the relative risk estimate is small and only 20% of cases of diabetes can be attributed to depression in people with both conditions. Further research is needed to determine possible causal mechanisms for the association and to ascertain whether depression and diabetes may have a common aetiology.     

Does HIV increase the risk of spousal violence in sub-Saharan Africa?

Although a positive association is found between HIV prevalence and intimate partner violence, a causal interpretation is hard to establish due to the endogeneity of HIV prevalence. Using the distance from the origin of the virus as an instrument, I find that an exogenous increase in HIV prevalence in a cluster has a sizable positive effect on the risk of physical and sexual violence against women within marriage. The results of this study confirm a gender-specific negative externality of the disease and encourage policy efforts to incorporate services for violence against women into existing HIV programs.     

Does ozonation of drinking water reduce the risk of bladder cancer?

BACKGROUND: Epidemiologic studies of drinking water disinfection byproducts have focused primarily on the carcinogenic potential of chlorination byproducts. Because drinking water has been ozonated in France for decades, we were able to assess the carcinogenic risk of the disinfection byproducts generated by both ozonation and chlorination. METHODS: We used data from a case-control study of bladder cancer conducted between 1985 and 1987 in 7 French hospitals. We compared 281 cases and 272 controls for whom we could reconstruct at least 70% of the residential exposure to drinking water contaminants over a 30-year period. RESULTS: When we took potential confounders and exposure to chlorination byproducts into account, the risk of bladder cancer decreased as duration of exposure to ozonated water increased (OR = 0.60 [95% CI = 0.3-1.3] for 1-9 years; OR = 0.31 [0.1-0.7] for 10 years or more). Simultaneously, the risk of bladder cancer increased with duration of exposure to chlorinated surface water and with the estimated trihalomethane content of the water. Our data suggest that ozonation reduces the risk associated with the chlorination of surface water and that ozonation alone could have an independent beneficial effect on bladder cancer risk. CONCLUSIONS: Our results are consistent with experimental evidence that ozonation in combination with chlorination decreases the concentration of trihalomethane in treated water and eliminates some of the mutagenicity of raw water.     

Does low maternal blood pressure during pregnancy increase the risk of perinatal death?

BACKGROUND: A recent report described an association between low maximum diastolic blood pressure (DBP) during pregnancy and perinatal death (stillbirth and death in the first week combined). The authors did not account for gestational length, a strong predictor of perinatal death. METHODS: We studied 41,089 singleton pregnancies from the U.S. Collaborative Perinatal Project (1959-1966). RESULTS: We observed an association between low maximum DBP and elevated risk of perinatal death. However, this association disappeared after accounting for reverse causation related to gestational length. At any given gestational week, women whose offspring ultimately experienced perinatal death did not have significantly lower maximum DBP than women whose offspring survived the perinatal period. When accounting for the trend of increasing DBP during late pregnancy through gestational-age-specific DBP standardized score, we saw no association between low diastolic blood pressure and perinatal death. CONCLUSIONS: Low maximum maternal DBP during pregnancy is a post hoc correlate of perinatal death, not a true risk factor.     

Does alcohol-use increase the risk of sexual intercourse among adolescents? Evidence from the NLSY97

This study investigates the causal link between alcohol-use and adolescent sexual activity. In a recent paper, using data from the 1995 wave of the National Longitudinal Study of Adolescent Health, Rees et al. [Journal of Health Economics 20 (5) (2001)] found little evidence of such a link. The data used here are from the National Longitudinal Study of Youth, 1997 (NLSY97), and results indicate that alcohol-use increases the probability of sexual intercourse, even after accounting for the potential endogeneity. However, consistent with Rees et al., there is less evidence that heavy drinking has a significant effect on sexual intercourse.     

Diffuse pleural fibrosis--an unreliable indicator of heavy asbestos exposure?

OBJECTIVES: This study aimed at testing the hypothesis that diffuse pleural fibrosis is associated with a heavier exposure to asbestos than that of benign pleural plaques, and hence diffuse pleural fibrosis can be used as a marker of heavy exposure. METHODS: Asbestos burden was estimated for 192 naval dockyard workers (96 with diffuse pleural fibrosis, 96 with plaques) by calculating the exposure ratings from the trade and the years spent in that trade. In 53 cases the diffuse pleural fibrosis was bilateral. RESULTS: No difference was found in the mean estimated asbestos burden between all diffuse pleural fibrosis and plaques, nor between plaques and unilateral and bilateral diffuse pleural fibrosis, analyzed separately by a one-factor analysis of variance. The mean asbestos burden was significantly greater for bilateral than for unilateral diffuse pleural fibrosis. A wide spread of asbestos exposure was noted among the men with diffuse pleural fibrosis. CONCLUSIONS: Diffuse pleural fibrosis may arise after widely varying exposure to asbestos. The mean exposure ratings for diffuse pleural fibrosis do not differ from those for pleural plaques, although the ratings are significantly higher for men with bilateral diffuse pleural fibrosis than for those with unilateral diffuse pleural fibrosis. Diffuse pleural fibrosis cannot be used as a reliable marker of heavy asbestos exposure.     

Does obesity increase risk for iron deficiency? A review of the literature and the potential mechanisms

Increasing obesity is a major global health concern while at the same time iron-deficiency anemia remains common worldwide. Although these two conditions represent opposite ends of the spectrum of over- and under-nutrition, they appear to be linked: overweight individuals are at higher risk of iron deficiency than normal-weight individuals. Potential explanations for this association include dilutional hypoferremia, poor dietary iron intake, increased iron requirements, and/or impaired iron absorption in obese individuals. Recent evidence suggests obesity-related inflammation may play a central role through its regulation of hepcidin. Hepcidin levels are higher in obese individuals and are linked to subclinical inflammation; this may reduce iron absorption and blunt the effects of iron fortification. Thus, low iron status in overweight individuals may result from a combination of nutritional (reduced absorption) and functional (increased sequestration) iron deficiency. In this review, we focus on subclinical inflammation in obesity, and its effect on hepcidin levels, as the most plausible explanation for the link between iron deficiency and obesity.