NIH: Viruses in Nondisinfected Drinking Water from Municipal Wells and Community Incidence of Acute Gastrointestinal Illness
June 2, 2016
NIH: Neurobehavioral Deficits and Increased Blood Pressure in School-Age Children Prenatally Exposed to Pesticides
June 2, 2016
Show all

NIH: Mortality in Young Adults following in Utero and Childhood Exposure to Arsenic in Drinking Water

Allan H. Smith, 1 Guillermo Marshall, 2, 3 Jane Liaw, 1 Yan Yuan, 1 Catterina Ferreccio, 2 and Craig Steinmaus1, 4

  • Background: Beginning in 1958, the city of Antofagasta in northern Chile was exposed to high arsenic concentrations (870 µg/L) when it switched water sources. The exposure abruptly stopped in 1970 when an arsenic-removal plant commenced operations. A unique exposure scenario like this—with an abrupt start, clear end, and large population (125, 000 in 1970), all with essentially the same exposure—is rare in environmental epidemiology. Evidence of increased mortality from lung cancer, bronchiectasis, myocardial infarction, and kidney cancer has been reported among young adults who were in utero or children during the high-exposure period.

    Objective: We investigated other causes of mortality in Antofagasta among 30- to 49-year-old adults who were in utero or ≤ 18 years of age during the high-exposure period.

    Methods: We compared mortality data between Antofagasta and the rest of Chile for people 30–49 years of age during 1989–2000. We estimated expected deaths from mortality rates in all of Chile, excluding Region II where Antofagasta is located, and calculated standardized mortality ratios (SMRs).

    Results: We found evidence of increased mortality from bladder cancer [SMR = 18.1; 95% confidence interval (CI): 11.3, 27.4], laryngeal cancer (SMR = 8.1; 95% CI: 3.5, 16.0), liver cancer (SMR = 2.5; 95% CI: 1.6, 3.7), and chronic renal disease (SMR = 2.0; 95% CI: 1.5, 2.8).

    Conclusions: Taking together our findings in the present study and previous evidence of increased mortality from other causes of death, we conclude that arsenic in Antofagasta drinking water has resulted in the greatest increases in mortality in adults < 50 years of age ever associated with early-life environmental exposure.

Millions of people worldwide are exposed to arsenic in their drinking water, and arsenic is a well-documented cause of many serious health effects. The International Agency for Research on Cancer (2004) classified arsenic in drinking water as carcinogenic to humans, based on evidence that arsenic causes cancers of the skin, lung, and bladder. Chronic arsenic exposure has also been shown to cause noncancer health outcomes in multiple organs, including reproductive, cardiovascular, pulmonary, neurologic, and dermal effects (National Research Council 1999, 2001). In the present study we investigated all causes of death following probable in utero and early-life exposure to arsenic.

We examined mortality in an area in northern Chile that has some unique features that make it an ideal location to study long-term outcomes from arsenic exposure. It is the driest inhabited place on earth (McKay et al. 2003). Because it had no private wells, all residents drank water from the only available source: the city water supply. Antofagasta obtained drinking water from rivers that flow from springs in the Andes Mountains. Before 1958, the arsenic level of the city water supply was about 90 µg/L. In 1958, a new city water supply was installed using water from the Toconce and Holajar rivers, which contained 800 and 1, 300 µg/L of arsenic, respectively (Smith et al. 1998). With these new sources of water, the average arsenic concentration in the city water supply increased dramatically to 870 µg/L. After a water treatment plant was installed in 1970, the arsenic concentration in the city water supply dropped to 110 µg/L for about 10 years and was reduced further thereafter. The water supply now contains < 10 µg/L of arsenic.

In previous studies of mortality among adults 30–49 years of age, we discovered increased mortality due to lung cancer and bronchiectasis (Smith et al. 2006), kidney cancer (Yuan et al. 2010), and acute myocardial infarction (Yuan et al. 2007) among residents born during or shortly before the high-exposure period. We therefore decided to extend our analysis to assess mortality from all causes of death among adults 30–49 years of age who were born during or before the high-exposure period. Because the age range of 30–49 years is a young age at which to die, we refer to these deaths as deaths in “young adults.”