Ortega García et al. Journal of Medical Case Reports 2011, 5:129 http://www.jmedicalcasereports.com/content/5/1/129 B6 (1.31 mg) and vitamin B12 (30.8 μg). Vitamin B12 and folate intake supplements were started on approxi- mately days 42 to 48 of gestation. Discussion In general, a careful PEH requires basic knowledge and instruction in order to orient and guide the anamnesis towards risk factors of the disease. An adequate training in PEH includes not only the theoretical aspects (such as knowing the related RFs), but also the ability to char- acterize and quantify exposures while communicating the pertinent risks and helping to avoid unnecessary alarm and/or omissions of relevant clinical information. This is especially important in cases such as ours, when a disease such as the autism spectrum was documented and may have been associated with exposures that had a high degree of uncertainty [6]. Initially, we conducted an extensive review of the lit- erature published since 1985 in PubMed Clinical Queries, Developmental and Reproductive Toxicology Database (DART) and Integrated Risk Assessment (IRIS). A selective search for chemicals in the Hazardous Substances Data Bank (HSDB) was also completed. The keywords used were: ‘Autism Spectrum Disorder’ OR ‘Autism’ AND ‘Risk Factor’. There was insufficient evi- dence to associate any chemical exposure to the diagno- sis of ASD, although there is some evidence suggesting that some prenatal factors increase the risk. Table 2 summarizes the environmental risk factors studied in the scientific literature that may increase the risk of developing the ASD. The causes for developmental disorders such as ASD are currently unknown. Genetic factors may provide some explanation. However, there is overwhelming evi- dence that environmental exposures during the period prior to conception and gestational weeks two to six are critical periods. Unfortunately, these are the periods of time when, in the majority cases, the pregnancies are still unrecognized by the prospective parents. Of importance in this case, maternal ethanol consump- tion continued until early gastrulation although physical features of fetal alcohol syndrome were not observed. Alcohol is a very potent toxin to the fetal nervous system and the relationship with autism remains controversial. It has been reported that up to 9% of children born to mothers that consume alcohol during pregnancy are autistic [7]. However, autistic symptoms per se are usually not considered to be part of fetal alcohol syndrome. However, recent case-control studies suggest that prena- tal alcohol exposure does not increase the risk of ASD [8]. Therefore, a strong association between prenatal alcohol exposure and autism is highly unlikely. Autism is common in populations exposed to a terato- genic insult around the time of gastrulation [9]. It is Page 3 of 5 now established that children with fetal alcohol spec- trum disorders (FASDs) display deficits in executive functioning (EF). Despite marked differences in their clinical presentation, children with autism also demon- strate pronounced deficits in EF. Therefore, it is reason- able to ask the question: is the pattern of executive deficits in FASDs different from that in autism? Occupational exposures of the mother and father of our patient were revised in DART and HSDB, but we found no relation with ASD and exposure effects during neurodevelopment. Horsetail remedies are not recommended for use dur- ing pregnancy or breastfeeding, since little information is available on their safety. Horsetail remedies have been known to cause neurodevelopmental toxicity, and have a high potential to cause thiamine depletion and nicotine- like effects [9-11]. Thiamine is water soluble and has a short half-life. Thiamine status can be altered due to: dietary thiamine deficiency, breakdown by thiaminase and the administration of thiamine analogues [12]. Recent phytochemical analyses have detected the pre- sence of tannins, saponins, sterols and flavonoids in horsetail residues [13-15]. In addition, horsetail contains thiaminase, an enzyme that destroys thiamine (vitamin B1) and, with long-term use, could lead to vitamin defi- ciency [11]. Thiaminase-induced deficiency of thiamine has been implicated to thiamine degradation by thermo- labile thiaminases present in raw fish and shellfish [16]. Plant thiamine antagonists are heat stable and occur as both orthohydroxyphenols and parahydroxyphenols. Some examples of these antagonists are caffeic acid, chlorogenic acid, and tannic acid. These compounds interact with thiamine to oxidize the thiazole ring, thus rendering it unable to be absorbed resulting in thiamine deficiency. Two flavonoids, quercetin and rutin, have also been implicated as thiamine antagonists [17]. Sev- eral spontaneous central nervous system disorders due to thiaminase effects have occurred in experimental ani- mal studies [18]. Horsetail remedies also contain diuretic properties used for weight control, which may explain our patient’s mother’s weight loss despite adequate caloric intake, an unusual occurrence in pregnant women. In our patient’s mother, the ingestion of B-complex vitamins did not reach the recommended daily allowance levels for preg- nant women (thiamine 1.4 mg/day, folic acid 600 μg/ day) and lactating women (thiamine 1.4 mg/day, folic acid 500 μg/day). Additionally, possible neurotoxicity caused by thiamine and folic acid deficiency could have been potentiated by the horsetail’s anti-thiamine activity and ethanol exposure during early pregnancy [11,18-20]. We believe that PEH is the best clinical tool to approximate the etiology of multi-factorial pediatric dis- eases. PEH is the basic and most essential work tool of