Rickets was the first environmental disease. Although it was first described in the 1600s, the disorder reached epidemic proportions by the end of the 1800s. Many children in industrialized Europe and North America began developing a variety of physical deformities including bow legs, pigeon chests, broad heads, and poor tooth development. Eventually scientists discovered that these abnormalities resulted from a deficiency of vitamin D. For urban children of past centuries, this deficiency was often caused by their living conditions. Sunless city streets darkened by industrial smog provided insufficient exposure to sunlight. However, the abnormalities associated with rickets and a related disorder, osteomalacia, have other etiologies in addition to vitamin D deficiency. Although treatments exist for some of these syndromes, others continue to present therapeutic challenges.
In 1645, Daniel Whistler published a thesis describing rickets. Unfortunately though, Francis Glisson defined rickets in a book in 1650. The book immediately became quite popular and Glisson's work quickly overshadowed that of Whistler (Gibbs 729-732).
Several centuries later, by the end of the 1800s, rickets had reached epidemic proportions. Indeed, scientists estimated that the majority of children living in the northern cities of England, Scotland, and Germany had developed rachitic abnormalities (Wilton 1516-1517). Such observations were confirmed by autopsy studies performed in Leiden, The Netherlands, which indicated that approximately 90 percent of the city's children had the disease (Holick 1-22). In the United States, rickets was also common in the large northern cities. For instance, Morse (1900) found evidence of rickets among approximately 80 percent Boston's infants and children under 2 years of age (Pitt 97-115).
While some blamed the epidemic on the dirty and crowded living conditions associated with industrial cities...