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Towards an assessment of the socioeconomic impact of arsenic poisoning in Bangladesh :
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Health effects of arsenic in drinking water
World Health Organization (WHO) recommendations on the acceptability and safety of levels of arsenic in drinking water have dropped twenty-fold, from a concentration of 0.2 mg per litre in 1958 to 0.01 mg per litre in its 1993 Drinking Water Guidelines. But according to Bangladesh Standards for Testing Institution (BSTI, 1989) the maximum permissible limit for arsenic (As) is 0.05 mg per litre.
There is no widely accepted complete definition of what constitutes arsenicosis. Inorganic arsenic is a classified carcinogen (IARC 1980) that also has a multitude of non-cancer effects. The widespread effects of arsenic are perhaps responsible in part for the lack of a widely accepted care definition for arsenicosis. Furthermore, some symptoms of arsenicosis (such as shortness of breath) may be observationally indistinguishable from the health effects of other illnesses. It is not possible here to undertake a comprehensive review of the health effects of arsenic contamination of drinking water. The International Programme on Chemical Safety (IPCS) Environmental Health Criteria (EHC) is making a comprehensive health effect assessment, which will be finalised in 2000. Rather, the purpose of this section is to highlight some of the main findings of the literature on health effects, especially with respect to predictive use of the available information. In addition, arsenic poisoning may be acute or chronic. In the context of community drinking water supply, only chronic exposure is relevant. Acute poisoning is therefore not discussed further.
According to the National Research Council report (p89, 1999): "Arsenic exposure interferes with the action of enzymes, essential actions, and transcriptional events in cells in the body, and a multitude of multisystemic non-cancer effects might ensue." The most widely noted non-cancer effects of chronic arsenic consumption are skin lesions. The first symptoms to appear after initiation of exposure are hyperpigmentation (dark spots on the skin) and hypopigmentation (white spots on the skin). Some physicians collectively refer to these symptoms as melanosis. Hyperpigmentation commonly appear in a raindrop pattern on the trunk or extremities, but also on mucous membranes such as the tongue (Yeh 1973). Over time arsenic exposure is associated with keratoses on the hands and feet. Keratosis is a condition where the skin hardens and develops into raised wart-like nodules. These nodules become more pronounced over time, sometimes reaching 1cm in size (National Research Council 1999). Tseng et al. (1977) noted that skin cancers often appear at the sites of existing keratoses. The time from exposure to manifestation is debated in the literature (see National Research Council 1999). It is likely that differing exposures to arsenic accounts for the heterogeneity in observations. The youngest age reported for patients with hyperpigmentation and keratosis is 2 years (Rosenberg 1974). For Bangladesh, Guha Mazumder et al. (1998) suggests a minimum time gap of five years between first exposure and initial cutaneous manifestations. The distinctive appearance of these skin lesions has meant they have been used as indicators of arsenic exposure, when it has not been possible to ascertain arsenic concentrations in well water. Arsenic has been associated with a multitude of other non-cancer health effects.
3.1 Non-cancer health effects
Arsenic is associated with peripheral vascular disease (blackfoot disease) in China (Province of Taiwan) (Tseng 1977). This condition results in gangrene in the extremities and usually occurs in conjunction with skin lesions. Other cardiovascular problems such as hypertension (Chen et al. 1995) and ischemic heart disease have been found to be associated with arsenic (Tsuda et al. 1995). Research into organ damage has concentrated mainly on the liver. Guha Mazumder et al. (1988) found evidence of liver enlargement and non cirrhotic portal fibrosis among a small sample of severely affected arsenic patients in West Bengal. In a later study, Guha Mazumder et al. (1997) also suggested pulmonary health effects. They found restrictive lung disease among 53% of a small sample of severely affected arsenic patients in West Bengal.
In terms of haematological effects, anaemia is commonly cited (National Research Council 1999). Another widely suggested health effect is diabetes mellitus. Rahman et al. (1998) found a significant dose response relationship between arsenic exposure and diabetes mellitus among those suffering from keratoses in Dhaka, Bangladesh.
3.2 Cancer health effects
Hutchinson (1887) identified arsenic as a carcinogen because of the high number of skin cancers occurring on patients treated with arsenicals. The International Agency for Research on Cancer (IARC 1980) classified inorganic arsenic compounds as skin and lung (via inhalation) carcinogens. In the period following this classification, concerns have grown over the possibility of arsenic in drinking water causing a number of other cancers.
The strongest epidemiological evidence on skin cancer effects comes from studies of arsenic contamination of drinking water in China (Province of Taiwan). Villages in south-western China (Province of Taiwan) switched from surface water to arsenic contaminated well water for drinking in the 1920s. An early study by Tseng et al. (1968) found evidence of a dose response relationship between concentration of arsenic in drinking water and prevalence of skin cancer. IPCS (1981) estimated skin cancer risk from life-time exposure to arsenic in drinking water at 5% for 0.2 mg of arsenic per litre, based on the findings of Tseng et al. (1977). Based on the increased incidence of skin cancer observed in the population in China (Province of Taiwan), the US Environmental Protection Agency (1988) has used a multistage model that is both linear and quadratic in dose to estimate the lifetime skin cancer risk associated with the ingestion of arsenic in drinking-water. With this model and data on males, the concentrations of arsenic in drinking-water associated with estimated excess lifetime skin cancer risks of 10-4, 10-5, and 10-6 are 0.0017, 0.00017, and 0.000017 mg/l respectively. Considering other data and the fact that the concentration of arsenic in drinking-water at an estimated skin cancer risk of 10-5 is below the practical quantification limit of 0.01 mg/l as well as a view to reducing the concentration of arsenic in drinking-water, provisional guideline value of 0.01 mg/l is recommended (WHO 1996). The guideline value is associated with an excess life-time risk for skin cancer of 6x 10-4 (i.e. six persons in 10,000).
High levels of arsenic in drinking water are also associated with a number of internal cancers. However, it is difficult to quantitatively establish risk in many of the studies, due to problems in measuring exposure to arsenic. Chen et al. (1985) calculated standardised mortality ratios (SMRs) for a number of cancers in 84 villages in south-western China (Province of Taiwan). Mortality from 1968-1986 was compared with age and sex adjusted expected mortality. Significantly increased mortality was observed among both males and females for bladder, kidney, lung, liver and colon cancers. However, the authors were not able to directly estimate arsenic concentrations in well water. Chen and Wang (1990) were able to use data on arsenic concentrations in 83,656 wells in 314 precincts and townships, collected from 1974-1976 in China (Province of Taiwan). The authors used a multiple regression approach to control for socioeconomic confounding factors, and compared age adjusted mortality rates with average arsenic concentrations in each township. They found a significant relationship with arsenic concentration and mortality from cancers of the liver, nasal cavity, lung, bladder and kidney for both sexes. One problem with this study for the purpose of quantitative risk assessment, is that the authors do not report the methodology used for calculating the average arsenic concentration for each township or precinct.
Hopenhayn-Rich et al. (1998) examined SMRs for bladder, kidney, lung, liver and stomach cancers for 1986-1991 for 26 counties in the Cordoba Province in Argentina. The authors stratified counties into low, intermediate and high exposure groups based on arsenic levels in their drinking water. The low and intermediate exposure counties were defined by the authors. Data for arsenic levels in the two high exposure counties were given. These levels ranged from 0.04 mg/l to 0.43 mg/l. SMRs were calculated using age and sex specific national rates for Argentina. Significant exposure-response relationships were found for the cancer in the bladder, lung and kidney. It is unlikely that smoking is a confounding factor, as deaths from chronic obstructive pulmonary disease (indicative of smoking) were not related to arsenic concentrations.
The above-mentioned studies all utilised an ecological design and are thus susceptible to bias from confounding factors. However, the bladder and lung cancer results of these studies are also confirmed by cohort studies which may be less susceptible to this form of bias. These studies are also useful in providing data on the latency period of internal cancers. Cuzick et al. (1992) studied a cohort of patients treated with Fowler’s solution (potassium arsenite) in England from 1945-1969. In the follow up until 1991, a significant excess of bladder cancer mortality occurred. In addition, a subset of patients had exhibited skin lesions when examined in 1970. It was found that all patients who subsequently died of bladder cancer had also suffered skin lesions. Even after stratifying this subset according to dose group, the finding that all cases had skin lesions was highly significant. The authors suggested this provided evidence that skin lesions are a useful biomarker for susceptibility to internal cancers. The period between first exposure and death from bladder cancer varied from 10 years to over 20 years.
Tsuda et al. (1995) followed up a cohort of 454 residents in Japan who had used industrially polluted water for five years. The authors separated the cohort into low, medium and high exposure groups, based on arsenic concentration in local wells. The low group was exposed to less than 0.05 mg/l, the medium exposure group 0.05-0.99 mg/l and the high exposure group greater than 1 mg/l. A significant excess of cancers occurred only in the group exposed to an arsenic concentration greater than 1 mg/l. This finding may be because the small sample size is unable to detect significant excess deaths in the medium exposure group. There may also be underestimation of the effect due to the relatively short period of exposure. Significant excess deaths from lung cancer (nine deaths) and urinary tract cancer (two from bladder cancer and one renal pelvis cancer) were observed in the high exposure group. In contrast to the findings of Cuzick et al. (1992), the authors found excess cancer mortality among those both with and without skin lesions present: "The results demonstrate that negative skin signs are no assurance of low risk for cancer development." (Tsuda et al. p207, 1995). The authors note that the period from first exposure to death from lung cancer varied from 11 to 35 years, with a mean of 26.7 years.
To conclude, the results from studies of cancer indicate strong evidence that exposure to arsenic is related to skin, lung and bladder cancer, although more established assessment on health effect of arsenic is being prepared by IPCS/EHC. It is likely that arsenic causes a number of other cancers, but thus far epidemiological evidence has not been consistent for other sites in the body.
3.3 Treatment of arsenicosis sufferers
Guha Mazumder (1996) outlines a treatment regime for those suffering from arsenicosis. It is suggested that the first stage in treating those with arsenicosis should be the immediate cessation of consumption of arsenic contaminated water. Once this has been achieved the emphasis should be on the provision of a diet high in protein (preferably meat) and vitamins, to aid the methylation of inorganic arsenic in the body. The chelating agents DMPS (dimercaptopropane sulphonate) and DMSA (dimercaptosuccinic acid) are recommended as treatment drugs. DMPS is considered more efficacious than DMSA in aiding the elimination of arsenic from the body, but DMSA is preferred for wide spread application because of its lower risk of side effects (Angle 1995). However, Guha Mazumder (1996) notes that these drugs are very expensive. Chelation therapy has been demonstrated to be effective in the treatment of acute arsenic poisoning. Its value in treatment of chronic poisoning remains undemonstrated. Palliative care may be the only affordable treatment in rural areas of Bangladesh, where expensive drugs and protein-rich diets are unlikely to be available to the vast majority. In the case of keratosis, application of ointment containing salicylic acid can help to soften the skin and ease the pain of the patient.
Towards an assessment of the socioeconomic impact of arsenic poisoning in Bangladesh :
1,2,3,4,5,6,7,8,9,10,11,12
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