Early knowledge on the toxicity of arsenicals has accumulated in Asian civilizations, where especially arsenic sulphide (realgar) had been traditionally used, both as a medicine and as a poison. According to Lewin (1929) such knowledge arrived at the Hellenic Mediterranean world following the conquests of Alexander the Great. Since then, there has been a continuous European history of both use of arsenic as a medicine and abuse as a homicide, until recently (Lewin 1929). For instance, Napoleon’s health began rapidly to fail in February 1821. He suffered from chronic As intoxication when he died on 5 May 1821, as now evidenced by analysis of his hair (Kintz et al. 2007; see Table 1). Biomonitoring of As in human hair is now regarded to be a useful tool in field studies evaluating chronically elevated As exposures (Pandey et al. 2007; Orloff et al. 2009; Kazi et al. 2011), although being less indicative at low (non-elevated) exposures (Cleland et al. 2009). Soluble inorganic arsenic is acutely toxic, and ingestion of large doses leads to gastrointestinal symptoms, disturbances of cardiovascular and nervous system functions, and eventually death. In survivors, bone marrow depression, haemolysis, hepatomegaly, melanosis, polyneuropathy and encephalopathy may be observed (WHO 2001). Chronic human exposure has been linked to a variety of dermal symptoms of arseni(c)osis (i.e. exfoliative dermatitis, keratosis, vitiligo, skin cancer), peripheral neuropathy, encephalopathy, bronchitis, pulmonary fibrosis, hepato-splenomegaly, portal hypertension, peripheral vascular disease/‘‘blackfoot disease’’, atherosclerosis, cancer (lung, urinary bladder, other organs) and diabetes mellitus (Pimparker and Bhave 2010). In contrast to its intentional use, arsenic as a chronic human environmental toxicant has an even much longer history by a couple of 1,000 years. At present, the oldest environmental exposure to arsenic is scientifically testified by hair analysis of the Tyrolean Neolithic mummy called ‘‘Otzi’’, who died between 3359 and 3105 BC (Oeggl 2009). In his case, copper enrichment near the hair surface and high arsenic contents in keratin cells of the interior of the hair shaft strongly argue in favour of a long-term involvement in copper working, accompanied by high arsenic exposure (Brothwell and Grime 2002). Table 1 compares these data with contemporary concentrations of arsenic in hair. Regarding historical aspects, a challenging theory is now being advanced that desertion of several important Etruscan settlements at the end of the Archaic period in Italy had been a consequence of man-made pollution and associated arsenic environmental poisoning (Harrison et al. 2010). According to the evaluation of WHO (2001), long-term exposure to arsenic in drinking water is causally related to increased risks of cancer in the skin, lungs, bladder and kidney, as well as other skin changes such as hyperkeratosis and pigmentation changes. These effects have been demonstrated in many studies using different study designs. Exposure–response relationships have been observed for each of these end-points. The effects have been most thoroughly studied in Taiwan, but there is considerable evidence from studies on populations in other countries as well. Increased risk of lung and bladder cancer and of