Type 1 diabetes—origins and epidemiology

In their Review, Norris and colleagues¹ state “Although many toxins have been introduced into the environment, many have been banned resulting in decreasing exposure trends.” However, environmental chemical exposure trends have actually been increasing overall, and are extremely consistent with temporal type 1 diabetes incidence trends.

In the USA and western Europe, the incidence of type 1 diabetes began to increase around the time of World War 2 (1939–45),² when industrial chemical production in these areas began.³ Since then, industrial chemical production has increased dramatically.³ Before 1939, when type 1 diabetes incidence rates were low, annual synthetic chemical production was also very low. However, by 2005, industrial chemical production had steadily increased to about 250 billion kg per year in the USA,³ and by this time the incidence of type 1 diabetes had also increased.¹

Although a handful of individual chemicals have been banned, these bans are largely restricted to some persistent organic pollutants. Environmental and human contamination remain widespread despite persistent organic pollutants declining over recent decades. All pregnant women in the USA have measurable concentrations of numerous chemicals across multiple bodily fluids, including many banned persistent organic pollutants.⁴ One reason environmental toxicology is so complex to study in humans is that no unexposed populations exist to serve as controls.

More than 350 000 chemicals and mixtures of chemicals are now registered for production and use worldwide, with more new chemicals added annually,⁵ yet we barely understand the health effects of a few hundred of these chemicals. The vast majority have never been studied for their metabolic toxicity, and almost none have been examined in relation to type 1 diabetes.