**1.7. Role of nutrition: food security**

The effect of several nutrients that can reduce arsenic toxicity has been studied. Oral supplementation with cysteine, methionine, vitamin C, and thiamin at a dose of 25 mg/ kg in studies in mice that were exposed to arsenic (10 ppm of sodium arsenite in drinking water) was observed a decrease in oxidative stress caused by exposure to arsenic, these nutrients were able to produce specific changes in the levels of lipid peroxidase, antioxidant enzyme activity and reduction in the concentration of arsenic in blood between 3 and 11%, in liver of 26–37%, and in kidneys from 16 to 24% (p < 0.05). Methionine and cysteine are the main amino acids that participate in the metabolism of arsenic, and vitamin C is an antioxidant [23, 27].

A case–control study conducted by Mitra et al. [28] in the adult population (n = 265) exposed to arsenic in drinking water (<500 μg/L) belonging to the city of West Bengal in India, found a higher probability of lesions due to exposure to arsenic associated with low protein intake (odds ratio = 1.94; CI: 95%, 1.05–3.59), calcium (OR = 1.89, 95% CI, 1.04–3.43), fiber (OR = 2.02, 95% CI, 1.15–4.21), and folic acid (OR = 1.67 95% CI, 0.87–3.2). In a study involving an adult population of 18–65 years (n = 1016), exposed to arsenic in drinking water in the city of Bangladesh, the consumption of some nutrients was quantified, finding that the ingestion of cysteine (950–2005 mg/d), methionine (1745–3530 mg/d), calcium (407–1500 mg/d), proteins (77–141 g/d), and vitamin B12 (2.3–9.9 μg/d) were associated with minors percentages of inorganic arsenic in urine, this speaks of a decrease in the total concentration of inorganic arsenic. Similarly, high ingestion of niacin and choline were associated with a higher rate of AMD to MMA (p = 0.02 for both cases), which indicates a higher conversion rate, and therefore, greater excretion of it [29]. A study developed in adult population (38 ± 10 years) (n = 130), evaluated the effect of folic acid on blood arsenic levels, the intervention consisted of an oral supplement of 400 μg/day of folic acid for 12 weeks. The authors found a decrease in the concentration of MMA in blood, going from 22.24 ± 2.86% in the intervention group and 1.24 ± 3.59% in the control group (p <0.0001). Total arsenic in blood was reduced by 13.62% in the intervention group, and 2.49% in the control group (p = 0.0199), as well as an increase in the rate of DMA excretion (p = 0.099), folic acid participates in methylation reactions [30, 31].

epithelial tissue, decreased production of red and white blood cells, central nervous system involvement, liver damage, and kidney damage [17, 22–24]. The acute lethal dose of arsenic

Exposure to arsenic generates oxidative stress, and this represents the main mechanism by which arsenic generates multi-organ damage, there are free radical formation directly and also inhibitory effects on antioxidant components [23]. An alteration in the metabolism of GSH secondary to the union of arsenic with -SH groups has been found, as well as the elevation of genes associated with oxidative stress such as heme oxygenase-1 and metallothioneins, after chronic exposure to arsenic [17, 26]. Chronic exposure to arsenic causes an increase in the production of reactive oxygen species (ROS) and an alteration in defense mechanisms against the pro-oxidative effect of ROS, mainly the catalase enzyme (CAT), superoxide dismutase

The effect of several nutrients that can reduce arsenic toxicity has been studied. Oral supplementation with cysteine, methionine, vitamin C, and thiamin at a dose of 25 mg/ kg in studies in mice that were exposed to arsenic (10 ppm of sodium arsenite in drinking water) was observed a decrease in oxidative stress caused by exposure to arsenic, these nutrients were able to produce specific changes in the levels of lipid peroxidase, antioxidant enzyme activity and reduction in the concentration of arsenic in blood between 3 and 11%, in liver of 26–37%, and in kidneys from 16 to 24% (p < 0.05). Methionine and cysteine are the main amino acids that participate in the metabolism of arsenic, and vitamin C is

A case–control study conducted by Mitra et al. [28] in the adult population (n = 265) exposed to arsenic in drinking water (<500 μg/L) belonging to the city of West Bengal in India, found a higher probability of lesions due to exposure to arsenic associated with low protein intake (odds ratio = 1.94; CI: 95%, 1.05–3.59), calcium (OR = 1.89, 95% CI, 1.04–3.43), fiber (OR = 2.02, 95% CI, 1.15–4.21), and folic acid (OR = 1.67 95% CI, 0.87–3.2). In a study involving an adult population of 18–65 years (n = 1016), exposed to arsenic in drinking water in the city of Bangladesh, the consumption of some nutrients was quantified, finding that the ingestion of cysteine (950–2005 mg/d), methionine (1745–3530 mg/d), calcium (407–1500 mg/d), proteins (77–141 g/d), and vitamin B12 (2.3–9.9 μg/d) were associated with minors percentages of inorganic arsenic in urine, this speaks of a decrease in the total concentration of inorganic arsenic. Similarly, high ingestion of niacin and choline were associated with a higher rate of AMD to MMA (p = 0.02 for both cases), which indicates a higher conversion rate, and therefore, greater excretion of it [29]. A study developed in adult population (38 ± 10 years) (n = 130), evaluated the effect of folic acid on blood arsenic levels, the intervention consisted of an oral supplement of 400 μg/day of folic acid for 12 weeks. The authors found a decrease in the concentration of MMA in blood, going from 22.24 ± 2.86% in the intervention group and 1.24 ± 3.59% in the control group (p <0.0001). Total arsenic in blood was reduced by 13.62% in the intervention

in humans has been estimated at 0.6 mg/kg/day [25].

(SOD), and glutathione peroxidase (GSH-Px) [23].

**1.7. Role of nutrition: food security**

46 Arsenic - Analytical and Toxicological Studies

an antioxidant [23, 27].

Zablotska et al. [32] studied 11,746 people over 18 years of age and found that consumption of riboflavin, pyridoxine, vitamin A, C, and E, and folic acid significantly modified the effects of arsenic exposure. Participants in the highest percentile of consumption of each nutrient (≥1.17 mg/d of riboflavin, ≥4.19 mg/d of pyridoxine, ≥351.61 μg/d of folic acid, ≥7113.06 mg/d of vitamin C, and ≥ 6.41 mg/d of vitamin E), showed a reduction in the risk of lesions derived from exposure to arsenic in 46–68% (p < 0.05). This reflects that the consumption of these key nutrients not only increase the excretion of arsenic, but also the reduction of adverse effects derived from exposure to As. In addition, it has been observed that the concentration of selenium in blood, which is an essential trace element required for the synthesis of several proteins, is inversely related to the risk of pre-malignant lesions in the skin, finding an inversely proportional relationship (p = 0.03) between the concentration of selenium in blood and arsenic in urine [8].

In addition to the above, a poor nutritional status, mainly malnutrition, correlates with the development of skin lesions caused by arsenic poisoning. In 2007 Maharjan et al. [33] developed a study in the adult population (n = 539) where an increase in the risk of manifesting skin lesions due to the arsenic exposure was found 1.65 times more in subjects with a body mass index (BMI) per below normal (16.5–17.1 kg/m<sup>2</sup> ) compared to those with a normal BMI (p < 0.05). In addition, it has been described that the decrease in BMI is also a non-specific manifestation of chronic exposure to high concentrations of arsenic (daily arsenic intake of 30 μg/kg/d). In rural populations, a low BMI is a reflection of a poor nutritional status, which is associated with a low intake of certain nutrients, including antioxidants, and nutrients whose poor ingestion has been related to increased production of MMA, the toxic form of arsenic, and a low production of DMA [30, 31, 34].
