The need for a reassessment of the safe upper limit of selenium in drinking water

Dettagli

Pubblicato Martedì, 15 Gennaio 2013 18:00

Vinceti M, Crespi CM, Bonvicini F, Malagoli C, Ferrante M, Marmiroli S, Stranges S.
Sci Total Environ. 2013 Jan 15;443:633-42 PMID: 23220755

Abstract

Results of recent epidemiologic studies suggest the need to reassess the safe upper limit in drinking water of selenium, a metalloid with both toxicological and nutritional properties. Observational and experimental human studies on health effects of organic selenium compounds consumed through diet or supplements, and of inorganic selenium consumed through drinking water, have shown that human toxicity may occur at much lower levels than previously surmised. Evidence indicates that the chemical form of selenium strongly influences its toxicity, and that its biological activity may differ in different species, emphasizing the importance of the few human studies on health effects of the specific selenium compounds found in drinking water. Epidemiologic studies that investigated the effects of selenate, an inorganic selenium species commonly found in drinking water, together with evidence of toxicity of inorganic selenium at low levels in from in vitro and animal studies, indicate that health risks may occur at exposures below the current European Union and World Health Organization upper limit and guideline of 10 and 40 μg/l, respectively, and suggest reduction to 1 μg/l in order to adequately protect human health. Although few drinking waters are currently known to have selenium concentrations exceeding this level, the public health importance of this issue should not be overlooked, and further epidemiologic research is critically needed in this area.

Leukemia risk in children exposed to benzene and PM10 from vehicular traffic: a case-control study in an Italian population

Dettagli

Pubblicato Mercoledì, 31 Ottobre 2012 18:04

Vinceti M, Rothman KJ, Crespi CM, Sterni A, Cherubini A, Guerra L, Maffeis G, Ferretti E, Fabbi S, Teggi S, Consonni D, De Girolamo G, Meggiato A, Palazzi G, Paolucci P, Malagoli C.
Eur J Epidemiol. 2012 Oct;27(10):781-90 PMID: 22892901

Abstract

Benzene, a recognized occupational leukemogen in adults, has been hypothesized to also increase the risk of childhood leukemia. We carried out a population-based case-control study in a northern Italy community involving 83 cases with acute childhood leukemia diagnosed in the years 1998-2009 and 332 matched controls. We assessed residential exposure to benzene and to particulate matter ≤10 μm (PM10) from motorized traffic using geocoded residences and detailed emission and dispersion modeling. Exposure to benzene, and to a lesser extent to PM10, appeared to be independently associated with an excess leukemia risk. When we stratified the study population by age and by leukemia subtype, the relative risk associated with benzene exposure was higher among children aged less than 5 years, and despite small numbers this relation appeared to be considerably stronger for acute myeloid leukemia than for acute lymphoblastic leukemia. Overall, these findings suggest that exposure to low levels of benzene released from motorized traffic may increase the risk of childhood leukemia, and suggest a possible independent effect of PM10, although unmeasured confounding due to other pollutants cannot be ruled out.

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Environmental risk factors for amyotrophic lateral sclerosis: methodological issues in epidemiologic studies

Dettagli

Pubblicato Mercoledì, 31 Ottobre 2012 18:02

Vinceti M, Fiore M, Signorelli C, Odone A, Tesauro M, Consonni M, Arcolin E, Malagoli C, Mandrioli J, Marmiroli S, Sciacca S, Ferrante M.
Ann Ig. 2012 Sep-Oct;24(5):407-15. PMID: 23193897

Abstract

The exact role of environmental risk factors in the etiology of the neurodegenerative disease amyotrophic lateral sclerosis (ALS) is still unknown. Their hypothetical contribution ranges from a minimal impact to a major role. Among the environmental factors strictu sensu (i.e., not life-style factors) suspected to play a role in ALS etiology, we consider pesticides, the metalloid selenium, some heavy metals, magnetic fields and cyanobacteria. However, the possibility exists that these factors exert their activity only in genetically susceptible persons and only after long-term exposures, thus further hampering epidemiologic studies. The recent availability of powerful tools such as population-based ALS registries for case ascertainment and clustering detection, and of environmental modeling techniques and of geographical information systems, may yield unique opportunities for offering insight into the etiology of the disease.

The environment and amyotrophic lateral sclerosis: converging clues from epidemiologic studies worldwide

Dettagli

Pubblicato Venerdì, 31 Agosto 2012 18:03

Vinceti M.
N Am J Med Sci. 2012 Aug;4(8):356-7. PMID: 22912944

Are environmental exposures to selenium, heavy metals, and pesticides risk factors for amyotrophic lateral sclerosis?

Dettagli

Pubblicato Martedì, 31 Luglio 2012 18:08

Vinceti M, Bottecchi I, Fan A, Finkelstein Y, Mandrioli J.
Rev Environ Health. 2012;27(1):19-41. PMID: 22755265

Abstract

The etiology of sporadic amyotrophic lateral sclerosis (ALS), the most common form of this degenerative disease of the motor neurons, is still unknown, despite extensive investigation of several genetic and environmental potential risk factors. We have reviewed laboratory and epidemiological studies assessing the role of exposure to neurotoxic chemicals (metalloid selenium; heavy metals mercury, cadmium, and lead; pesticides) in ALS etiology by summarizing the results of these investigations and examining their strengths and limitations. Despite limitations in the exposure assessment methodologies typically used in human studies, we found suggestive epidemiological evidence and biologic plausibility for an association between ALS and antecedent overexposure to environmental selenium and pesticides. The relation with mercury, cadmium, and lead appears weaker.