In the early 1990s, several groups of scientists—including epidemiologists and pneumologists—began to publish a series of prospective studies reporting an increased incidence of cardiovascular diseases in people exposed to low levels of airborne particles.1 ,2 Before these publications, toxicological studies had primarily focused on pulmonary effects of particulates in laboratory animals—and the results from those studies indicated that air pollution levels in many places were too low to cause harm to humans. This created something of a paradox, seemingly: epidemiologists finding adverse effects for which the biological mechanisms were not apparent. Over the next several years, the epidemiological and clinical evidence on cardiovascular effects associated with particulates increased,2 leading to the design of toxicological and other laboratory studies aiming at understanding mechanisms for the effects. Epidemiological data challenged assumptions and furthered knowledge about the mechanisms of toxicity. And ultimately, the toxicologists began asking and answering different questions. Laboratory and population studies were enriching each other, as they should. As a result, we now have a good understanding of cardiovascular risks from particulates, and have corresponding policies and regulation to protect citizens from air pollution.