Common enterovirus infections appear to initiate or facilitate the pathogenetic processes leading to type 1 diabetes (T1D) and also sometimes precipitate the clinical disease. We have recently demonstrated that (1) enterovirus-positive islet cells were seen on postmortem pancreatic specimens of several T1D patients but not in the corresponding samples of nondiabetic controls, and (2) several different enteroviruses can be associated with T1D. Enterovirus infections are transmitted from person to person by fecal–oral or respiratory routes, which means that infections usually start from the respiratory or gastrointestinal mucosa. Regardless of the clinical symptoms of the disease, viral replication continues in the submucosal lymphatic tissue for several weeks, up to a couple of months, and during that time the virus is excreted into the feces and translocated to the environment. Monitoring of sewage samples for enteroviruses can be used as a tool in epidemiologic studies of enterovirus. Finland has successfully used environmental control data in poliovirus surveillance for decades. About 24 samples have been collected annually from the Helsinki region, which covers about 20% of the population. In the present study, we have reanalyzed the sewage samples of the years 1993–2004 for nonpolio enteroviruses by inoculating them into five different continuous cell lines known to cover a wide range of serotypes. Isolated strains were identified by RT-PCR and VP1 sequencing. The most commonly detected serotypes were coxsackie B viruses (CBV1–5) and echoviruses (E6, 7, 11, 25, 30). Diabetogenic effects of the most prevalent enterovirus serotypes were studied in primary human β cells.