Toxic oil syndrome appeared in epidemic form in Spain in 1981. Epidemiologi
c studies have demonstrated that illness was caused by consumption of rapes
eed oil that had been denatured with aniline. Chemical analyses of oil spec
imens conducted in conjunction with epidemiologic studies have established
that consumption of specific oils containing fatty acid anilide contaminant
s was associated with increased risk for disease. New chemical analytic met
hods identified a family of compounds, the di-fatty acid esters of phenylam
ino propane diol, and one of these compounds, the 1,2 di-oleyl ester of 3-(
N-phenylamino)-1,2-propanediol (DPAP), has been found to be more strongly a
ssociated with disease status than the fatty acid anilides. We found the od
ds ratio for exposure to DPAP (OR = 26.4, 95% CI 6.4-76.3) is much higher t
han the odds ratio for exposure to oleyl anilide (OR = 4.1, 95% CI = 2.2-7.
8), implying that exposure to DPAP was a more relevant risk factor for deve
lopment of toxic oil syndrome than exposure to oleyl anilide. In this paper
, we review and present analyses of data from multiple studies of the possi
ble etiologic role of DPAP in toxic oil syndrome. The presence of DPAP in o
il collected from affected and unaffected households was a more specific co
rrelate of case relatedness than was the presence of fatty acid anilides, a
nd it was equally sensitive. Moreover, DPAP was found in oil from the only
refinery whose oil was clearly associated with illness.