Effect of High Aluminum Concentration in Water Resources on Human Health, Case Study: Biga Peninsula, Northwest Part of Turkey (original) (raw)
Related papers
Bmj, 1999
ObjectiveTo establish whether people exposed to drinking water contaminated with 20 tonnes of aluminium sulphate in the Camelford area of Cornwall in the south west of England in July 1988 had suffered organic brain damage as opposed to psychological trauma only.DesignRetrospective study of affected people.Participants55 affected people and 15 siblings nearest in age to one of the group but who had not been exposed to the contaminated water were studied.Main outcome measuresVarious clinical and psychological tests to determine medical condition and anxiety levels in affected people. Assessment of premorbid IQ (pFSIQ) with the national adult reading test, a computerised battery of psychomotor testing, and measurement of the difference in latencies between the flash and pattern visual evoked potentials in all participants.ResultsThe mean (SE) pFSIQ was above average at 114.4 (1.1). The most sensitive of the psychomotor tests for organic brain disease was the symbol digit coding (SDC) test (normal score 100, abnormal <85). Participants performed less well on this test (54.5 (6.0)) than expected from their pFSIQ (P<0.0001) and a little less poorly on the averaged less discriminating tests within the battery (86.1 (2.5), P<0.0001). In a comparison with the 15 sibling pairs (affected people’s age 41.0 (3.3) years v sibling age of 42.7 (3.1) years (P=0.36) the exposed people had similar pFSIQ (114.7 (2.1)) to their siblings (116.3 (2.1), (P=0.59) but performed badly on the symbol digit coding test (51.8 (16.6)) v (87.5 (4.9) for siblings, P=0.03). The flash-pattern differences in exposed people were greater than in 42 unrelated control subjects of similar age (27.33 (1.64) ms v 18.57 (1.47) ms, P=0.0002). The 15 unexposed siblings had significantly better flash-pattern differences than their affected siblings (13.4 (2.4) ms v 29.6 (2.9) ms, P=0.0002). No effect of anxiety could be shown on these measurements from the analysis of the anxiety scores of exposed people.ConclusionPeople who were exposed to the contaminated water at Camelford suffered considerable damage to cerebral function, which was not related to anxiety. Follow up studies would be required to determine the longer term prognosis for affected individuals. Key messagesAluminium is a well established neurotoxinAccidental contamination of drinking water in Camelford by aluminium sulphate led to symptoms of loss of concentration and short term memory that were initially attributed to anxietyIn residents exposed to the contaminated water psychomotor performance was poorer than predicted from premorbid IQ and the difference between flash-pattern visual evoked potentials was greater than normalAnxiety did not influence either of these measures of cerebral functionAluminium sulphate poisoning probably led to long term cerebral impairment in some people in Camelford
Review of epidemiologic studies of aluminium and neurological disorders
Environmental Geochemistry and Health, 1990
The epidemiological study of neurological disorders is just beginning and should he continued because of the potential public health impact of these diseases on society. The most important contribution of epidemiologicai research is the identification of risk factors, and specific disease entities, such as Alzheimer's disease, should be studied. Ecological analysis of geographical data have associated a small increase in mortality from Alzheimer's disease and dementia with the aluminium content of drinking water. These results must necessarily be interpreted with caution because serious errors may result from inferences based on ecological analysis, e.g. "the ecologic fallacy". Potential risk factors for Alzheimer's disease have been studied in case-comparison epidemiology studies conducted in Italy, Massachusetts, Colorado, Minnesota and North Carolina, but only two studies have considered aluminium exposure, through the use of antacids. Although no increased risk was found to be associated with aluminium exposure, only a small number of individuals in the studies reported antacid use, and the studies had an extremely limited statistical power to detect an association. Additional analytical epidemiology studies, either cohort or case-comparison, are required to better describe the possible relationship between aluminium and Alzheimer's disease. These studies should be designed according to well-established epidemiological principles, be conducted with no selection bias and minimum observation bias, consider potential confounding and modifying factors, and have sufficient statistical power to enable detection of low relative risks.
Peripheral neuropathy induced by drinking water contaminated with low-dose arsenic in Myanmar
Environmental Health and Preventive Medicine, 2019
Background: More than 140 million people drink arsenic-contaminated groundwater. It is unknown how much arsenic exposure is necessary to cause neurological impairment. Here, we evaluate the relationship between neurological impairments and the arsenic concentration in drinking water (ACDW). Participants and methods: A cross-sectional study design was employed. We performed medical examinations of 1867 residents in seven villages in the Thabaung township in Myanmar. Medical examinations consisted of interviews regarding subjective neurological symptoms and objective neurological examinations of sensory disturbances. For subjective neurological symptoms, we ascertained the presence or absence of defects in smell, vision, taste, and hearing; the feeling of weakness; and chronic numbness or pain. For objective sensory disturbances, we examined defects in pain sensation, vibration sensation, and two-point discrimination. We analyzed the relationship between the subjective symptoms, objective sensory disturbances, and ACDW. Results: Residents with ACDW ≥ 10 parts per billion (ppb) had experienced a "feeling of weakness" and "chronic numbness or pain" significantly more often than those with ACDW < 10 ppb. Residents with ACDW ≥ 50 ppb had three types of sensory disturbances significantly more often than those with ACDW < 50 ppb. In children, there was no significant association between symptoms or signs and ACDW. Conclusion: Subjective symptoms, probably due to peripheral neuropathy, occurred at very low ACDW (around 10 ppb). Objective peripheral nerve disturbances of both small and large fibers occurred at low ACDW (> 50 ppb). These data suggest a threshold for the occurrence of peripheral neuropathy due to arsenic exposure, and indicate that the arsenic concentration in drinking water should be less than 10 ppb to ensure human health.
Unusual neuropathological features and increased brain aluminium in a resident of Camelford, UK
Neuropathology and applied neurobiology, 2017
The possible role of aluminium in the pathogenesis of Alzheimer's disease (AD) has been hotly debated over the past few decades. Whereas the so-called "aluminium hypothesis" was popular in the 1970s and 1980s it has gradually fallen out of favour in the past few years possibly following a number of inconclusive and contradictory human environmental/clinical studies. Nevertheless, there have from time to time been reminders in the media of environmental accidents; these have prevented the topic from disappearing completely from public memory. This article is protected by copyright. All rights reserved.
Environmental geochemistry and health, 1990
Comparisons of maps and correlation and regression analysis indicate a geographical association between aluminium (AI) in drinking water and registered death rateswith dementia (coded from death certificates as the underlying or a contributory cause of death) in Norway. High levels of AI in drinking water are in most cases related to acid precipitation. In general, correlations between aggregate environmental measurements and mortality are a weak source of evidence for risk factors for disease, however, and interpretations regarding cause-and-effect relationships should therefore be made with great care. The major uncertainty probably relates to the use of registered death rates with dementia as a measure of incidence rates of Alzheimer's disease. The dementia rates are correlated with population density, and it is possible that the association between AI and dementia might be due to differences in diagnosis and reporting of dementia. Thus, the present study can only be regarded as introductory, and further epidemiological studies are needed to help elucidate the role of AI in Alzheimer's disease. The results provide little evidence of an association between AI in drinking water and Parkinson's disease or amyotrophic lateral sclerosis. < ,,
Metabolic Brain Disease
The conceptualisation of autistic spectrum disorder and Alzheimer's disease has undergone something of a paradigm shift in recent years and rather than being viewed as single illnesses with a unitary pathogenesis and pathophysiology they are increasingly considered to be heterogeneous syndromes with a complex multifactorial aetiopathogenesis, involving a highly complex and diverse combination of genetic, epigenetic and environmental factors. One such environmental factor implicated as a potential cause in both syndromes is aluminium, as an element or as part of a salt, received, for example, in oral form or as an adjuvant. Such administration has the potential to induce pathology via several routes such as provoking dysfunction and/or activation of glial cells which play an indispensable role in the regulation of central nervous system homeostasis and neurodevelopment. Other routes include the generation of oxidative stress, depletion of reduced glutathione, direct and indirect reductions in mitochondrial performance and integrity, and increasing the production of proinflammatory cytokines in both the brain and peripherally. The mechanisms whereby environmental aluminium could contribute to the development of the highly specific pattern of neuropathology seen in Alzheimer's disease are described. Also detailed are several mechanisms whereby significant quantities of aluminium introduced via immunisation could produce chronic neuropathology in genetically susceptible children. Accordingly, it is recommended that the use of aluminium salts in immunisations should be discontinued and that adults should take steps to minimise their exposure to environmental aluminium.
2006
This study was designed to assess the effects of exposure to arsenic in drinking water on neurosensory function. A questionnaire including neurological signs and symptoms and a brief neurological exam consisting of pinprick testing of the arms and legs and knee-jerk test were administered to 321 residents of the Bamen region of Inner Mongolia, China. Arsenic in water was measured by hydride generation atomic fluorescence. Participants were divided into three exposure groups-low (non-detectible-20), medium (100-300) and high (400-700 mg/l) arsenic.