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Arsenic High Blood Pressure PDF Print E-mail

Arsenic-related High Blood Pressure


Context - Arsenic is a poisonous substance, which is released both from certain human activities and naturally from the Earth's crust.

Humans may be exposed to arsenic mainly through food and water, particularly in certain areas where the groundwater is in contact with arsenic-containing minerals.

To what extent can arsenic exposure affect human health or the environment?


What happens to arsenic absorbed by the body?

The amount of arsenic absorbed into the body from inhaled airborne particles is highly dependent on two factors, the size of particles and their solubility. The size of the particles determines how far into the lungs they can penetrate – the further they penetrate the more likely arsenic is to be absorbed. The solubility of the particles in the fluid lining the lungs determines how easily arsenic will be absorbed into the blood stream. In the gut, soluble arsenic compounds from food and beverages are rapidly and extensively absorbed into the blood stream.

In humans and most common laboratory animals, inorganic arsenic is metabolized via two main types of reaction: (1) conversion of the pentavalent form of arsenic - arsenate - to the trivalent form - arsenite, and (2) methylation, i.e. addition of a methyl group comprising one atom of carbon and three of hydrogen (-CH3) to the trivalent form. After methylation arsenic can be rapidly eliminated from the body with the urine. There can be large differences between individual humans in their capacity for methylation that is most likely due to differences in enzyme capacity in the body. It is not clear if children have a reduced capacity for methylation compared with adults. Studies suggest that the main pathway for getting rid of arsenic from the body, methylation, may be inhibited at high exposures.

The uptake and elimination of arsenic depends on its chemical form, particularly at high exposures. For example, ingested organic arsenic compounds are much less extensively metabolized and more rapidly eliminated in urine than inorganic arsenic in both laboratory animals and humans. In the case of inorganic arsenic, the trivalent forms pass more rapidly into the tissues compared with the pentavalent forms.


The source document for this Digest states:

Kinetics and metabolism

Absorption of arsenic in inhaled airborne particles is highly dependent on the solubility and the size of particles. Both pentavalent and trivalent soluble arsenic compounds are rapidly and extensively absorbed from the gastrointestinal tract. In many species arsenic metabolism is characterized by two main types of reactions: (1) reduction reactions of pentavalent to trivalent arsenic, and (2) oxidative methylation reactions in which trivalent forms of arsenic are sequentially methylated to form mono-, di- and trimethylated products using S-adenosyl methionine (SAM) as the methyl donor and glutathione (GSH) as an essential co-factor. Methylation of inorganic arsenic facilitates the excretion of inorganic arsenic from the body, as the end-products MMA and DMA are readily excreted in urine. There are major qualitative and quantitative interspecies differences in methylation, to the extent that some species exhibit minimal or no arsenic methylation (e.g. marmoset monkey, guinea-pig, chimpanzee). However, in humans and most common laboratory animals, inorganic arsenic is extensively methylated and the metabolites are excreted primarily in the urine. Factors such as dose, age, gender and smoking contribute only minimally to the large inter-individual variation in arsenic methylation observed in humans. However, lower methylation efficiency in children has been observed in only one study out of three. Studies in humans suggest the existence of a wide difference in the activity of methyltransferases, and the existence of polymorphism has been hypothesized. Animal and human studies suggest that arsenic methylation may be inhibited at high acute exposures. The metabolism and disposition of inorganic arsenic may be influenced by its valence state, particularly at high dose levels. Studies in laboratory animals indicate that administration of trivalent inorganic arsenic such as As2O3 and arsenite initially results in higher levels in most tissues than does the administration of pentavalent arsenic. However, the trivalent form is more extensively methylated, leading to similar long-term excretion. Ingested organoarsenicals such as MMA, DMA and arsenobetaine are much less extensively metabolized and more rapidly eliminated in urine than inorganic arsenic in both laboratory animals and humans.


The extremely high exposure levels evaluated in prior investigations relating elevated levels of drinking water arsenic and hypertension prevalence make extrapolation to potential vascular effects at lower exposure levels very difficult. A cross-sectional study was conducted on 8790 women who had recently been pregnant in an area of Inner Mongolia, China known to have a gradient of drinking water arsenic exposure. This study observed increased systolic blood pressure levels with increasing drinking water arsenic, at lower exposure levels than previously reported in the literature. As compared to the referent category (below limit of detection to 20 μg of As/L), the overall population mean systolic blood pressure rose 1.29 mm Hg (95% CI 0.82, 1.75), 1.28 mm Hg (95% CI 0.49, 2.07), and 2.22 mm Hg (95% CI 1.46, 2.97) as drinking water arsenic concentration increased from 21 to 50, 51 to 100, and > 100 μg of As/L, respectively. Controlling for age and body weight (n = 3260), the population mean systolic blood pressure rose 1.88 mm Hg (95% CI 1.03, 2.73), 3.90 mm Hg (95% CI 2.52, 5.29), and 6.83 mm Hg (95% CI 5.39, 8.27) as drinking water arsenic concentration increased, respectively. For diastolic blood pressure effect, while statistically significant, was not as pronounced as systolic blood pressure. Mean diastolic blood pressure rose 0.78 mm Hg (95% CI 0.39, 1.16), 1.57 mm Hg (95% CI 0.91, 2.22) and 1.32 mm Hg (95% CI 0.70, 1.95), respectively, for the overall population and rose 2.11 mm Hg (95% CI 1.38, 2.84), 2.74 mm Hg (95% CI 1.55, 3.93), and 3.08 mm Hg (95% CI 1.84, 4.31), respectively, for the adjusted population (n = 3260) at drinking water arsenic concentrations of 21 to 50, 51 to 100, and > 100 μg of As/L. If our study results are confirmed in other populations, the potential burden of cardiovascular disease attributable to drinking water arsenic is significant.

Keywords: Arsenic; Drinking water; Blood pressure; Cardiovascular disease; Post-natal; Reproductive health; Women; Inner Mongolia, China

Last Updated on Friday, 05 August 2011 12:42