Exposure to persistent organic pollutants (POPs) is of concern in Arctic populations since these contaminants accumulate in fish and marine mammals, which is an important part of the traditional diet of these populations. Epidemiological and experimental studies have reported significant associations between POPs and increased blood pressure (BP) in populations with different degrees of exposure.
We aimed to assess the risk of hypertension related to increasing levels of polychlorinated biphenyls (PCBs) and organochlorine (OC) pesticides.
Fifteen PCBs and 11 OC pesticides or their metabolites were determined in plasma of 1614 Inuit adults = 18 years living in 9 towns and 13 villages in Greenland. BP was measured using a standardized protocol. The risk of hypertension was estimated through logistic regression using POPs as continuous variables (log-transformed). Hypertension was defined as systolic BP = 140 mm Hg, diastolic BP = 90 mm Hg and/or antihypertensive treatment.
Overall, the odd ratios (ORs) of hypertension were not statistically significant for dioxin-like PCBs, non-dioxin-like PCBs and OC pesticides after adjusting for confounders. Once the analyses were stratified by age category (18-39 and = 40 years), increased risk of hypertension was observed for total dioxin-like PCBs among the youngest [OR: 1.34 (95% CI: 1.03-1.74)] while a borderline protective effect was observed for total non-dioxin-like PCBs [OR: 0.81 (95% CI: 0.66-0.99)] among the oldest. Higher risk of hypertension was also associated with increasing p,p'-dichlorodiphenyltrichloroethane (DDT) concentrations among the youngest [OR: 1.42 (95% CI: 1.08-1.85)].
Overall, no significant associations were observed between PCBs, OC pesticides and blood pressure in this highly exposed population although the associations differed by age category.
Acid precipitation may increase human exposure to several potentially toxic metals by increasing metal concentrations in major pathways to man, particularly food and water, and in some instances by enhancing the conversion of metal species to more toxic forms. Human exposures to methylmercury are almost entirely by way of consumption of fish and seafood. In some countries, intakes by this route may approach the levels that can give rise to adverse health effects for population groups with a high consumption of these food items. A possible increase in methylmercury concentrations in fish from lakes affected by acid precipitation may thus be of concern to selected population groups. Human exposures to lead reach levels that are near those associated with adverse health effects in certain sensitive segments of the general population in several countries. The possibility exists that increased exposures to lead may be caused by acid precipitation through a mobilization of lead from soils into crops. A route of exposure to lead that may possibly be influenced by acid precipitation is an increased deterioration of surface materials containing lead and a subsequent ingestion by small children. A similar situation with regard to uptake from food exists for cadmium (at least in some countries). Human metal exposures via drinking water may be increased by acid precipitation. Decreasing pH increases corrosiveness of water enhancing the mobilization of metal salts from soil; metallic compounds may be mobilized from minerals, which may eventually reach drinking water. Also, the dissolution of metals (Pb, Cd, Cu) from piping systems for drinking water by soft acidic waters of high corrosivity may increase metal concentrations in drinking water. Exposures have occasionally reached concentrations which are in the range where adverse health effects may be expected in otherwise healthy persons. Dissolution from piping systems can be prevented by neutralizing the water before distribution. Increased aluminum concentrations in water is a result mainly of the occurrence of Al in acidified natural waters and the use of Al chemicals in drinking water purification. If such water is used for dialysis in patients with chronic renal failure, it may give rise to cases of dialysis dementia and other disorders. A possible influence on health of persons with normal renal function (e.g., causing Alzheimer's disease) is uncertain and requires further investigation.(ABSTRACT TRUNCATED AT 400 WORDS)
Methylmercury (MeHg) exposure has been linked to an increased risk of coronary heart disease (CHD). Paraoxonase 1 (PON1), an enzyme located in the high-density-lipoprotein (HDL) fraction of blood lipids, may protect against CHD by metabolizing toxic oxidized lipids associated with low-density liproprotein and HDL. MeHg has been shown to inhibit PON1 activity in vitro, but this effect has not been studied in human populations.
This study was conducted to determine whether blood mercury levels are linked to decreased plasma PON1 activities in Inuit people who are highly exposed to MeHg through their seafood-based diet.
We measured plasma PON1 activity using a fluorogenic substrate and blood concentrations of mercury and selenium by inductively coupled plasma mass spectrometry in 896 Inuit adults. Sociodemographic, anthropometric, clinical, dietary, and lifestyle variables as well as PON1 gene variants (rs705379, rs662, rs854560) were considered as possible confounders or modifiers of the mercury-PON1 relation in multivariate analyses.
In a multiple regression model adjusted for age, HDL cholesterol levels, omega-3 fatty acid content of erythrocyte membranes, and PON1 variants, blood mercury concentrations were inversely associated with PON1 activities [?-coefficient = -0.063; 95% confidence interval (CI), -0.091 to -0.035; p