The extent of underground water contamination
In the present study, the arsenic contamination in water was evaluated using the groundwater samples collected from various adjoining villages of Kaurikasa of Rajnandgaon district in Chhattisgarh. Twenty water samples were collected from eight villages, including Kaurikasa. Table 1 summarises the obtained results. Total arsenic was above the permissible limit in eighteen samples of five villages. The geogenic distribution of arsenic was found variable in the region, which might be due to the variable geochemical system. An examination of the results shows that the water sample from Kaurikasa village recorded (AS III-980±126.08μg/L; AS V- 1220±120.06) was the highest of all samples, which could be due to the greater depth of the borewell compared to the handpump samples from the same village. In the descending order, the arsenic levels (in μg/L) in groundwater samples were Bharritola (ASIII-432±28.6 and 232±15.3; AS V 604±36.06 and 386±24.02), Kuretola (ASIII-212+14.8; AS V- 348±21.06), Mangatola (ASIII-160±9.8; AS V- 230±36.02), and Tumrikasa (ASIII-150±9.6; AS V-216±16.04). Out of three samples collected from Murhetola, two samples were within permissible limits ASIII43±0.06; ASV-78±6.07 μg/L and ASCII-47±4.02; ASV-84±5.18 μg/L, respectively (Table-01). The arsenic level in groundwater samples in Kaurikasa and surrounding villages is far above the limit of 10 μg/L recommended by WHO for drinking water (WHO, 1999).
Symptomatic features of Arsenicosis among the population of Kaurikasa
The survey was carried in association with a physician among the population of Kaurikasa village who confirmed the highest degree of Arsenicosis. The study revealed a prevalence of various symptoms of Arsenicosis among people, as described below:
- Diffused type of melanosis with darkening of the skin in various parts of the body, especially on the palm.
- Spotted melanosis of face, hand, limb, back, and chest.
- Patches of melanosis on the tongue, gum, and lips
- Diffused and nodular keratosis on the palm and sole.
- Leucomelanosis on several parts of the body.
- Hepatomegaly, splenomegaly and ascitis.
- Non-pitting swelling.
- General weakness, sleeplessness, breathlessness, and indigestion are common complaints from the people in the affected area (Fig 1a, b, c & d).
Hematological alterations among the population suffering from Arsenicosis
Based on prevailing symptoms, twenty people (12–62 years) were selected for hematological and biochemical evaluation from Kaurikasa village. The Hemoglobin percentage was found below the normal range in nineteen samples and RBC count was found low in thirteen samples. WBC was lower in eleven samples, but ESR was found high (>20 mm/h) in sixteen samples in comparison to their normal range. PCV and platelet count were lower in twelve than their standard limit, but prothrombin time was elevated in eighteen samples relative to their standard limit. (Fig. -3)
Belon et al. (2006) reported a low count of RBC, WBC, and low estimation of PCV, Hemoglobin, but a high level of ESR among the population in the groundwater arsenic-contaminated village of Ghetugachhi (Chakdha, West Bengal, India). Soignet et al. in 2001 have also observed the mitostatic effect of arsenic trioxide, especially for WBC in patients with relapsed acute promyelocytic leukemia (APL). Winski et al. in 1997 have established hemolysis and destruction in Hemoglobin in human blood exposed to arsine, and they found an alteration in the volume control of cells due to leakage of potassium and influx of sodium which increased hematocrit. Blair et al. (1990) investigated the impact of arsine gas exposure on male and female mice for 5, 15, and 90 days. They reported moderate hemolytic anemia, evident by a decrease in erythrocyte counts, hematocrits, and hemoglobin concentration. Tripathi et al. (2003) have reported a significant fall in hemoglobin concentration and PCV along with a decrease in total erythrocyte count in a Clarias batrachus after exposure to sodium arsenite and observed the disturbed hemopoiesis, erythrocyte membrane disruption, impaired iron uptake by RBC, and hemolysis due to arsenic toxicity. The Agency of Toxic substances and Disease Registry (ATSDR), Atlanta in 2000, in a case study of 35 years human of chronic Arsenicosis reported the occurrence of macrocytic anemia, bone marrow depression, a low percentage of hematocrit, leucopenia, and thrombocytopenia. Wilkinson et al. (1975) also reported thrombocytopenia in the human population suffered from chronic exposure to arsenic. In China, the use of arsenic for the treatment of leukemia is an age-old practice. In an incident in China in 2004, over a hundred workers ingested extensive levels of arsenic due to an accident caused by pipeline leakage in a copper smelting factory. After toxicological evaluation, Yuanyuan Xu et al. found 69.2% of sufferers were Leucopenic within 15 days. Similarly, in Taiwan, 926 workers of semiconductor plants were investigated by Luo et al. (1995) of which 30% of male photolithography workers were found Leucopenic than 5-6% in control male workers. Our findings for the twenty people exposed to arsenic-contaminated groundwater are almost in concurrence with the earlier reports from different parts of the world.
Biochemical alterations among the population suffering from Arsenicosis
The biochemical alterations noticed in the twenty blood samples were found significant. The serum glucose was below the normal range in ten samples (Fig. 4). Among lipid profiles the total cholesterol, LDL and HDL were found above the normal range in eight, eighteen, and thirteen samples respectively, but the TG was above the normal range in all twenty samples (Fig. 5). Protein metabolism was also disturbed. The total protein, albumin, and globulin levels were found below the normal range in nineteen, twenty, and sixteen samples, respectively (Fig. 6). The total bilirubin and creatinine were higher than the normal range in fifteen and sixteen samples, respectively (Fig. 7). The serum urea level was above the standard limit in all twenty samples (Fig. 8). SGOT was within the normal limit in all twenty samples, but SGPT was above the normal range in all twenty samples. Alkaline phosphatase was below the normal range in all twenty samples (Fig. 9). Pal et al. in 2004 have reported a hypoglycemic effect in male Wistar rats, similar to our findings. Mukherjee et al. (2004), Navas-Acien et al. (2006), and Zierold et al. (2002) have also reported hyperglycemia under arsenic poisoning. Acute arsenic toxicity, including its effect on glucose metabolism, is generally associated with its reactivity towards the thiol (SH) group (Aphoshian 1989; HRC 1999). Under acute conditions, arsenite inhibits the enzyme pyruvate and alpha-ketoglutarate dehydrogenase (Aposphian 1989) which is necessary for glucogenesis and glycolysis processes. Krebs in early 1993 also described that arsenic interferes with pyruvic acid metabolism. Arsenate, on the other hand, can mimic phosphate during energy transfer pathways of phosphorylation and it is also involved in oxidative phosphorylation uncoupling (Kennedy and Lahninger 1949). However, it is unlikely that these toxic effects of acute arsenic exposure take place as a result of chronic exposure to environmentally relevant doses (Tseng 2004). Arsenic could influence alteration in sugar metabolism by other mechanisms, including oxidative stress, inflammation, apoptosis, and the nonspecific mechanism that has been involved in the pathogenesis of type-2 diabetes. Arsenic exposure can augment the production of reactive oxygen species (Chen et al. 1998, Tseng 2004, Wang et al. 1996), impede the activity of crucial antioxidant enzymes such as glutathione reductase, glutathione-S- transferase, glutathione peroxidase, and glucose-6-phosphate dehydrogenases (Maiti and Chatterjee 2000; Santra et al. 2000) and also can induce lipid peroxidation (Santra et al. 2000). In studies from Taiwan, the increase in arsenic levels in human blood is correlated with the increased level of reactive oxygen species and with increasing levels of antioxidant capacity of plasma (Wu et al. 2001). Overall the experimental and epidemiological evidence at present is insufficient to confirm the arsenic-induced hyperglycemia or hypoglycemia.
In the present study, we found raised levels of total cholesterol, HDL, LDL, and TG in a majority of samples. In a study conducted in Bangladesh in the arsenic-contaminated region, overall 45% of residents were reported with a low range of total cholesterol, 54% with low range of HDL, and 20% with low range of LDL but triglyceride was above the normal range of 47% population (Nabi et al. 2005). Several studies suggest no significant changes in lipid profile due to arsenic toxicity (Want et al. 2006; Petia et al. in 2003; Mahaffey et al. 1977). Protein metabolism was also found disturbed in the present study (Fig. 6). In a study where arsenic contamination in drinking water was established, the total protein in serum was found higher in 43% population (Nabi et al. 2005). In an experiment conducted on the pigs, the total protein concentration was found to decrease than the normal range (Wang et al. 2006). The oxidative stress ensuing from arsenic toxicity causes damage to sulfur-containing enzymes and other proteins. This phenomenon ends up in the form of inactivation of protein, defective cross-linkages, and protein denaturation (Serhan et al. 1991). Serum albumin and a small fraction of globulin are synthesized in the liver, and the serum protein is afflicted both quantitatively and qualitatively in liver disorder. In any disease-causing hepato-cellular damage, the concentration of serum albumin decreases. The dynamically changing levels of serum albumin, therefore, are a valuable indicator of severity, progress, and prognosis in hepatic diseases. In the present study, liver cell damage is attributed due to arsenic toxicity.
The elevated levels of bilirubin were observed in the current study. In plasma, bilirubin is found as indirect reacting bilirubin which is insoluble in water. The direct reacting esterified bilirubin is water-soluble. At the end of the life, span erythrocytes are destroyed in the reticuloendothelial system and liberate hemoglobin. The globulin is separated from Hemoglobin, and the porphyrin ring is opened. The released iron part goes into the iron store and may be used further for hemoglobin synthesis. Green color biliverdin forms first from the non-iron-containing residue of Hemoglobin (i.e. Protoporthyrin). Biliverdin gets reduced to yellow-colored bilirubin. Generally, total serum bilirubin is found to increase in case of hepato-cellular damages (toxic hepatopathy neoplasm, etc.), obstructions in intra and extrahepatic biliary tract, intravascular, and extravascular hemolysis processes. Excessive elevation of direct bilirubin is seen during cholestasis and late in the course of chronic liver diseases. In the present finding, an elevated level of bilirubin in 16 samples out of 20 suggests liver toxicity among the population due to Arsenicosis.
The elevated level of SGPT in all 20 samples also suggests liver cell damage. Steven et al. in 2001 and Wang et al. in 2006 have also reported an increased concentration of SGPT under Arsenicosis. While serum urea was elevated in all the 20 samples, the creatinine level was high in 16 samples. Belon et al. also reported a high concentration of serum urea and creatinine in a study on 20 males and 19 females affected by groundwater arsenicosis in village Dasdiya of West Bengal, India. Elevated levels of urea are found in pre-renal, renal, and post-renal conditions associated with high serum creatinine in any renal functional impairment. Thus the current finding of both high urea and creatinine levels indicates renal dysfunction among the population due to Arsenicosis.
In the present study, alkaline phosphatase activity was found lowered in all twenty samples. Mahaffey et al. (1977) and Mehranjani et al. (2006), have also reported the decreased activity of alkaline phosphatase under Arsenicosis, but Mazumdar et al. (1998) found increased activity in 51.3% of patients suffering from Arsenicosis in West Bengal, India. Thus our results endorse the findings of Mehranjani et al., that under the influence of Arsenicosis, the activity of alkaline phosphatase is impaired.
Table– 1- Distribution of arsenic in Kaurikasa and nearby villages of Rajnandgaon district of Chhattisgarh, India (Number of sample replicates = 10)
Sample Number
|
Village
|
Source
|
Depth of water tapping points (Ft.)
|
Estimated Concentration of As III (μg/L) [Mean±SD]
|
Estimated Concentration of As V (μg/L) [Mean±SD]
|
1.
|
Murhetola
|
Hand Pump
|
280
|
57.00±4.03
|
106.00±8.04
|
2.
|
Murhetola
|
Hand Pump
|
260
|
43.00±3.06
|
78.00±6.07
|
3.
|
Murhetola
|
Hand Pump
|
262
|
47.00±4.02
|
84.00±5.18
|
4.
|
Devasur
|
Hand Pump
|
268
|
55.00±4.06
|
92.00±6.06
|
5.
|
Devasur
|
Hand Pump
|
276
|
55.00±4.06
|
88.00±6.04
|
6.
|
Tumrikala
|
Hand Pump
|
262
|
62.00±4.8
|
98.00±7.06
|
7.
|
Tumrikala
|
Hand Pump
|
350
|
150.00±9.6
|
216.00±16.04
|
8.
|
Kuretola
|
Hand Pump
|
364
|
212.00±14.8
|
348.00±21.06
|
9.
|
Bharritola
|
Hand Pump
|
372
|
232.00±15.3
|
386.00±24.02
|
10.
|
Bharritola
|
Hand Pump
|
400
|
432.00±28.6
|
604.00±36.06
|
11.
|
Kaurikasa
|
Borewell
|
480
|
980.00±126.08
|
1220.00±120.06
|
12.
|
Kaurikasa
|
Hand Pump
|
275
|
55.00±4.07
|
86.00±6.04
|
13.
|
Kaurikasa
|
Hand Pump
|
340
|
73.00±18.03
|
124.00±16.08
|
14.
|
Dongargaon
|
Well
|
320
|
54.00±4.05
|
96.00±8.02
|
15.
|
Dongargaon
|
Hand Pump
|
300
|
59.00±4.6
|
102.00±8.08
|
16.
|
Dongargaon
|
Hand Pump
|
270
|
54.00±4.04
|
88.00±6.06
|
17.
|
Dongargaon
|
Hand Pump
|
262
|
57.00±4.04
|
84.00±5.06
|
18.
|
Dongargaon
|
Hand Pump
|
260
|
54.00±4.03
|
80.00±4.08
|
19.
|
Dongargaon
|
Hand Pump
|
275
|
62.00±4.6
|
92.00±6.02
|