No abstract

The etiologic agent(s) that was responsible for the 1981 toxic oil syndrome [TOS] epidemic in Spain has not been identified. Liquid chromatography combined with atmospheric pressure ionization tandem mass spectrometry was used for the analysis of oils associated with TOS. Analyses focused on measuring 3-(N-phenylamino)-1,2-propanediol [PAP], the 3-oleyl ester of PAP [MEPAP], and the 1,2-di-oleyl ester of PAP [DEPAP]. DEPAP and MEPAP were found more frequently and at higher concentrations in TOS case-associated oils than in control oils with odds ratios of 13.7 (95% CI 5.0-38) and 21.9 (95% 6.1-78), respectively. Other fatty acid esters of PAP are also likely to be present in the TOS case-associated oils. More significantly, DEPAP and MEPAP were found in aniline-denatured rapeseed oil refined at ITH, the oil refining company with the clearest link to TOS cases, yet these PAP esters were not detected in unrefined aniline-denatured samples of rapeseed oil delivered to ITH. These results show that the esters of PAP were products of the ITH refining process and were not formed spontaneously during storage. PAP esters were not detected in samples of other aniline-denatured rapeseed oils that were refined elsewhere, and which were not associated with illness. These findings provide strong support for the hypothesis that one or more of the fatty acid esters of PAP were the etiologic agents for TOS.

This paper summarizes the deliberations of a work group charged with addressing specific questions relevant to risk estimation in developmental neurotoxicology. We focused on eight questions. a) Does it make sense to think about discrete windows of vulnerability in the development of the nervous system? If it does, which time periods are of greatest importance? b) Are there cascades of developmental disorders in the nervous system? For example, are there critical points that determine the course of development that can lead to differences in vulnerabilities at later times? c) Can information on critical windows suggest the most susceptible subgroups of children (i.e., age groups, socioeconomic status, geographic areas, race, etc.)? d) What are the gaps in existing data for the nervous system or end points of exposure to it? e) What are the best ways to examine exposure-response relationships and estimate exposures in vulnerable life stages? f) What other exposures that affect development at certain ages may interact with exposures of concern? g) How well do laboratory animal data predict human response? h) How can all of this information be used to improve risk assessment and public health (risk management)? In addressing these questions, we provide a brief overview of brain development from conception through adolescence and emphasize vulnerability to toxic insult throughout this period. Methodological issues focus on major variables that influence exposure or its detection through disruptions of behavior, neuroanatomy, or neurochemical end points. Supportive evidence from studies of major neurotoxicants is provided. Key words: abnormal neurological development, behavioral teratology, behavioral testing methodology, delayed neurotoxicity, developmental disorders, developmental neurotoxicology, environmental health, neurobiological substrates of function, neuronal plasticity. -Environ Health Perspect 1 08(suppl 3): 535-544 (2000). http.//ehpnetl.niehs.nih.gov/docs/2000/suppl-3/535-544adams/abstract.html

In 1996, a citizens group in Nogales, Arizona, reported to the Arizona Department of Health their concerns about a possible excess prevalence of systemic lupus erythematosus (SLE) due to exposure to environmental contamination in the area. The authors conducted a two-phase study in which the objectives of phase I were to identify potential SLE cases and to determine the prevalence of SLE and the objectives of phase II were to identify potential risk factors associated with the development of SLE and to evaluate the possible association between SLE and environmental exposure to pesticides and inorganic compounds. Participants included 20 confirmed cases and 36 controls. The authors found the prevalence of SLE to be 103 cases per 100,000 population (95 percent confidence interval: 56, 149), two to seven times higher than the prevalence in the US population. They detected elevated levels of 1,1-dichloro-2,2-bis-(p-chorophenyl)ethylene and organophosphate metabolites among cases and controls. In both, levels were higher than the reference mean for the US population. The authors found no statistical association between elevated levels of pesticides and disease status. Their results show that the prevalence of SLE in Nogales is higher than the reported prevalence in the US population and that both cases and controls had past exposure to chlorinated pesticides and have ongoing exposure to organophosphates.