Once arsenic compounds are absorbed, the liver’s metabolic pathway processes and converts them into different types of inorganic and organic species (Chung et al, 2014). These are then quickly absorbed into the blood and circulated to the human gastrointestinal tract. Organic arsenic is less absorbed based on the poor absorptive quality of the species whilst inorganic arsenic species are highly reactive and cause a series of intracellular reactions. The metabolites of arsenic are eventually by the major excretion pathway for the elimination of arsenic species from the body – urine.
The effects of arsenic exposure are divided into four stages Abdul et al (2015). They are preclinical, clinical, internal complications and malignancy stages. An outline of these stages can be found in the figure below:
Fig. 2. Stages of clinical manifestations in arsenic toxicity.
Arsenic in the body can affect all major organ systems.
Abdul et al (2015) highlights that the type of arsenic exposure dictates the development of clinical symptoms.
In acute arsenic toxicity organ damage could occur and may lead to early death whilst chronic exposure may lead to the development of malignant tumors and subsequently death. Arsenic has been classified as a group-1 carcinogen by the International Agency for Research on Cancer (IARC) as it has shown the ability to induce tumorigenesis in humans in skin, lung, bladder, liver, and prostates in exposed organisms. The diagram below shows the major organ systems that are affected by arsenic.
Fig. 1. The key effects of arsenic on major organ systems.
The following table further outlines the observations of the effects of arsenic on different body systems, highlighted by Abdul et al (2015).
Integumentary (Dermal) System As it is the largest organ system, it is considered to be more susceptible to the effects of arsenic exposure. In fact, arsenicosis is manifested this way. Skin lesions usually develop after exposure. Other signs of excess arsenic exposure is the formation of distinct white lines in nails and alopecia. Fig 3 in the appendix outlines the major dermatological signs and symptoms of arsenic exposure.
Nervous System Due to the absorptive potential of arsenic into blood, it can easily cross the blood brain barrier and get distributed in the brain. The highest accumulation is observed in the pituitary gland and neurologic complications are generally quick. The ultimate stage is neurotoxicity and the steps are outlined in Figure 4 below.
Respiratory System Inhalation of arsenic in air often produces respiratory complications. It has also been observed that chronic arsenic exposure by either drinking water or occupational source may lead to respirational complications.
Cardiovascular System High arsenic exposure is associated with cardiovascular diseases (CVD) and their risk factors (i.e. atherosclerosis, hypertension, arrhythmia and diabetes). Arsenic exposure increases the reactive oxygen species and oxidative stress causing decrease in bioavailability of nitric oxide. On the other hand, arsenic exposure increases its interaction with the sulfhydryl groups and obstruct metabolism in the cells. Both these consequences independently lead to the development of endothelial insufficiency, increased expression of cytokines, inflammatory mediators and atherosclerotic genes causing atherogenesis and other cardiovascular complications.
Hematopoietic System Immediately after exposure, arsenic enters into systemic circulation and affects bone marrow, spleen and erythrocytes. Majority of the arsenic primarily binds to hemoglobin and accumulates in the erythrocytes and this leads to the development of anemia.
Immune System Arsenic has been seen to have detrimental effects on the immune system of exposed organism including immunosuppression. It does this by inhibition the production of or induce proliferation of immune cells in a dose dependent manner. Immunotoxicity generally results from the inhibition of the function of human macrophages as well as the development of monocytes. Arsenic is capable of inducing a range of autoimmune diseases including diabetes, atherosclerosis and non-melanoma skin cancers. It also impairs the development, activation, proliferation and function of lymphocytes and prolonged exposure to arsenic may increase the expression of inflammatory molecules in the body.
Hepatic System Due to the liver being a metabolic site, accumulation of arsenic there is relatively higher and the liver becomes prone to increased hepatic toxicity. Some of the early clinical symptoms of hepatic toxicity include bleeding from esophageal varices, ascites, jaundice or enlargement of liver. Liver disease and subsequently damage usually follows.
Chronic exposure to arsenic generally causes cirrhosis, ascites, and liver cancer.
Endocrine System Arsenic is a well-known disruptor of parts of the endocrine system including the thyroid, thyroid hormone, pancreas, gonads and the hypothalamic-pituitary-adrenal axis.
It accumulates in pancreas and decreases the secretion of insulin as well as viability of the cell. The insufficient insulin produced is one of the major causes of diabetes especially Type 2 Diabetes Mellitus, the form which results when there is a development of insulin resistance in the body.
Gastrointestinal symptoms such as nausea, vomiting and diarrhea are commonly associated with arsenic exposure. Initial clinical signs of acute or sub-acute arsenic induced gastrointestinal disturbances including excessive salivation, nausea, thirst, burning lips, swallowing problems, gastrointestinal cramps, abdominal pain, dehydration and severe diarrhea were reported.
Renal System As arsenic is eliminated through the renal system, an accumulation of it leads to cytotoxicity in renal tissue. This then manifests as hypourea, elevated levels of serum creatinine, blood urea nitrogen and proteinuria which is followed by renal injury. Arsenic may cause damage to capillaries and glomeruli of kidney and significantly impair the renal function.
Reproductive System Arsenic is a well-known teratogen which affects the development of fetus. The dose and duration of arsenic exposure influences growth retardation and fetal death. It also affects sex organs and may cause fertility issues in both genders.
As a non-mutagenic human carcinogen, arsenic induced tumorigenesis is one of the most common human diseases influenced by epigenetic modifications. Gene methylation changes also result and these are capable expressing oncogenes and/or downregulate tumor suppressor genes.\n
Adverse effects on health and the environment (include data)
Abdul et al. (2015) states that approximately 100 million people all around the world are exposed to arsenic levels more than 50 μg/L via drinking water and industrial processes. In an effort to address a closer relationship, Chung et al. (2014) states that it is necessary to identify and quantify each chemical form of arsenic to evaluate their individual effects on human health. After all, the toxicity of arsenic is strongly dependent on the type of chemical species present in the body.
In many countries across the world, we see where there are links made between the high levels of arsenic in the environment and the health of its residents. On the continent of Africa, reports have shown that health concerns reported in some African countries are associated with smoke from mines and food crops grown in mining contaminated areas. From as early as 1975, villagers close to the Obuasi gold mine in Ghana, claim to have developed chronic eye inflammation as a result of the mine smoke (Amasa 1975). Furthermore, Amasa (1975), Amonoo Neizer and Amekor (1993), and Adomako et al. (2010) have reported high concentrations of aresnic in food items such as orange, sugar cane, cassava, and rice from mining regions in Ghana. Smedley et al. (1996) had highlighted a link between the concentrations of inorganic urinary arsenic from sample populations and drinking water in Ghana. They found that a rural stream-water-drinking community has a mean value of 42 μgL −1 of urinary arsenic whilst a suburb of Obuasi community using groundwater for potable supply has 18μgL−1. In Burkina Faso, health surveys have also identified skin lesions characterized by melanosis, keratosis, and ulceronecrotic tumor in patients from three villages where high-As groundwaters have been found (COWI 2005; Smedley et al. 2007). Recent reports have suggested that two deaths linked to high-As drinking water have occurred in this area (Ouedraogo 2006). Besides, Somé et al. (2012) identified that 29.26 and 46.34 % of the population (240 persons) in 20 villages in Yatenga province, Burkina Faso, were affected by melanosis and keratosis, respectively. According to them, this public health problem in Yatenga linked to arsenic is due to drinking water. Indeed, they found that 52 % of the water samples exceeded the WHO guideline value (10 μgL −1) whilst no trace of arsenic was found in the samples of tomatoes, cabbages, and potatoes.
As arsenic is easily transferred, Ahoulé et al. (2015) studied the relationship between the uptake or arsenic into leafy vegetables. What was found was that vegetables grown in soil with high total arsenic had high arsenic levels and vice-versa. The graph below shows that.
Fig. 2 Measured concentrations of As (mg/kg, dry wt basis) in leafy greens grown on the urban (Albany) and orchard (G6) soils amended with phosphate, Fe oxide, peat and gypsum
Zandsalimi et al (2011) carried out a similar test and concluded that the plant species tested had an arsenic content which positively correlated to that of the soil.
Due to the adverse effects of arsenic on health and the environment, measures have been investigated and are even place to reduce the impact of pollution.
Kord Mostafapour et al. (2010) investigated the use of dissolved air flotation to remove arsenic from water. That study concluded that the method is highly efficient if poly aluminum chloride is used as a coagulant. Ahoulé et al. (2015) reviewed articles related the removal or arsenic from waters in Africa. One article (Ebina et al. 2003) examined the synthesis and arsenic adsorption capability of smectite-titanium oxide nanocomposite of tunable pore size. The results of the study show that a clay-titanium oxide nanocomposite synthesized from smectite powder and titanium oxide powder has a good adsorption capability of arsenic (III) and As (V) dissolved in water. The second article (Bowell, 1994) deals with the sorption of arsenic by iron oxides and oxyhydroxides in soils. The results showed that the iron oxides and oxyhydroxides coming from neutral-pH oxidized clay-rich soils and oxidized surface portion of mine tailing soils at the Ashantimine, Ghana, adsorb arsenic more than that coming from highly acidic soils or reducing conditions and the organic-rich soils. Though the technologies assessed have some advantages, there are some concerns as their by-products can be a further potential source for secondary arsenic pollution.
In 2017, Wang et al. published the results of a study of equipping coal fired power plants in the US and China with various air pollution control devices. The results of that was that on average, over 90% of arsenic in the flue gas wass captured by the dry particulate matter collection system with less than 3% of arsenic remaining in the boiler slag, and another 3% captured by the desulfurization system. 1% was captured by wet precipitators and the remainder was emitted from the stack. The study also showed that ultralow-emission technology with a low-temperature economizer before the electrostatic precipitator (ESP) promoted the capture of more arsenic compounds. Reactions between arsenic and the denitrification catalyst made it difficult to reach a perfect arsenic mass balance in a power plant, excluding plants that are equipped with a hot ESP installed before the selective catalytic reduction system.