Chromosomal aberrations and sister chromatid exchanges in individuals exposed to arsenic through drinking water in West Bengal, India

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Abstract

Arsenic contamination in groundwater has become a worldwide problem. Currently an unprecedented number of people in West Bengal, India and Bangladesh are exposed to the ubiquitous toxicant via drinking water in exposure levels far exceeding the maximum recommended limit laid down by WHO. This arsenic epidemic has devastated nine districts of West Bengal encompassing an area of 38,865 km2 leading to various clinical manifestations of chronic arsenicosis. We conducted a human bio-monitoring study using chromosomal aberrations (CA) and sister chromatid exchanges (SCE) as end points to explore the cytogenetic effects of chronic arsenic toxicity in the population of North 24 Parganas, one of the arsenic affected districts in West Bengal. Study participants included 59 individuals residing in this district where the mean level (±S.E.) of arsenic in drinking water (μg/l) was 211.70±15.28. As age matched controls with similar socio-economic status we selected 36 healthy, asymptomatic individuals residing in two unaffected districts—Midnapur and Howrah where the mean arsenic content of water (μg/l) was 6.35±0.45. Exposure was assessed by standardized questionnaires and by detecting the levels of arsenic in drinking water, nails, hair and urine samples. In the exposed group the mean arsenic concentrations in nails (μg/g), hair (μg/g) and urine (μg/l) samples were 9.04±0.78, 5.63±0.38 and 140.52±8.82, respectively, which were significantly high (P<0.01) compared to the corresponding control values of 0.44±0.03, 0.30±0.02 and 5.91±0.49, respectively. Elevated mean values (P<0.01) of the percentage of aberrant cells (8.08%) and SCEs per cell (7.26) were also observed in the exposed individuals in comparison to controls (1.96% and 5.95, respectively). The enhanced rates of CAs and SCEs among the residents of North 24 Parganas are indicative of the cytogenetic damage due to long term exposure to arsenic through consumption of contaminated water.

Introduction

Arsenic is an established human carcinogen causing lung tumors by inhalation, and cancers of the skin and bladder by ingestion [1], [2]. Arsenic contamination from the leaching of mining deposits and emissions from industries have been reported in countries like USA, Japan, UK and Australia, while arsenic in natural aquifers used for drinking water supply has affected millions of people in India, Bangladesh, China, Chile, Hungary, Mexico, Argentina, Thailand, and Taiwan. With respect to human health impact, the situation is very serious in West Bengal, India and Bangladesh [3], [4] and seems to occur at lower levels of exposure as compared to native Atacamenos in Chile and Argentina [5], [6]. Till January 1999, 9 out of 18 districts in West Bengal have been found to be affected by arsenic, encompassing an area of 38,865 km2 with concentration of arsenic in groundwater ranging from 200 to 800 μg/l [7]. According to the latest survey, 300,000 people already have arsenic induced skin lesions and a larger number of people are suspected to be sub-clinically affected [8]. Endemic arsenicism in West Bengal is associated with hyperpigmentation, keratosis of skin, anemia, burning sensation of the eyes, solid edema of the legs, liver fibrosis, chronic lung disease, gangrene of the toes (blackfoot disease) and neuropathy [9].

We have reviewed and updated the existing data on mutagenic and genotoxic effects of arsenic [10]. Arsenic has been found to be a paradoxical human carcinogen which does not cause point mutations but is clastogenic in both animal and human systems. Increased incidences of CAs, SCEs and micronuclei (MN) have been reported from the human populations exposed to arsenic through drinking water in various countries such as Mexico [11], [12], Finland [13], Argentina [14], [15], Hungary [16], and USA [17]. These human biomonitoring studies prove that arsenic is an active inducer of CAs, whereas the findings with respect to SCEs have been questioned [6], [15]. Very recently we published the first study on the cytogenetic effects of arsenic exposure in West Bengal, where we reported an enhanced frequency of MN in lymphocytes, oral mucosa and urothelial cells of symptomatic individuals exposed to arsenic through drinking water in this area [18]. The present study is aimed at evaluation of the incidence of cytogenetic damage as measured by the frequencies of CAs and SCEs in the symptomatic individuals exposed to arsenic through drinking water in the district of North 24 Parganas, West Bengal, India (see Fig. 1).

Section snippets

Study design and group selection

The arsenic exposed population was selected from the residents of four villages (designated as 3–6 in Fig. 1) located within 5 km radius in North 24 Parganas, one of the arsenic affected districts. A cohort of 59 residents (37 males and 22 females) with symptoms of arsenicism like hyperpigmentation, hypopigmentation, hyperkeratosis, raindrop pigmentation or ulcerative lesions was recruited for both CA and SCE assays (see Fig. 2, Fig. 3, Fig. 4, Fig. 5). The study participants were examined by

Statistical methods

The significance of the differences between arsenic contents obtained in the exposed and control groups was calculated by Fisher’s t-test. CA and SCE assays were also analyzed using Fisher’s t-test and the level of significance is presented in the respective tables.

Results

Table 1 shows the total arsenic contents in drinking water, nails, hair and urine samples as well as the frequencies of CA and SCE of the exposed individuals while data on the same parameters for the control group are presented in Table 2. The results show a marked difference as regards to exposure to arsenic through drinking water in both the groups. Table 3, Table 4 represent the mean results (±S.E.) of the arsenic contents and the CA frequencies (including and excluding gaps), respectively.

Discussion

In the present study, results of CA and SCE assays of the symptomatic individuals clearly show a significant increase of cytogenetic damage in the lymphocytes due to exposure to arsenic through drinking water. The percentage of aberrant cells in lymphocytes of exposed individuals showed nearly a four-fold increase as compared to controls. Out of all types of aberrations, chromatid breaks and gaps were the predominant forms of CAs observed. Chromosome type aberrations such as dicentrics were

Acknowledgements

We are extremely grateful to Dr. P.K. Sarkar, the Director and all the staff members of the Skin Outpatient Department, School of Tropical Medicine for their kind cooperation and help to collect the biological samples from the arsenic skin lesion patients. We are also grateful to the Director, Indian Institute of Chemical Biology for his kind help and cooperation to continue this study. We are thankful to the Council of Scientific and Industrial Research, Government of India, for providing

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