Children chemical agent exposure

Other approaches to induce gastrointestinal discomfort have far more serious toxic effects. The chemical colchicine stops cell division (an antimitotic), producing severe nausea, vomiting, and dehydration, which can lead to delirium, neuropathy, and kidney failure. On the other hand, colchicine is used in the treatment of gout and has been studied as an anticancer agent because it stops cell division. Most toxic of all are plants that produce lectins, and the most toxic of these is the chemical ricin produced by castor beans. Only 5 to 6 seeds are necessary to kill a small child. Fortunately, following oral consumption much of the ricin is destroyed in the stomach. Ricin is extremely effective at stopping protein synthesis, so much so that direct exposure to only 0.1 pg/kg can be fatal. 

The younger child and toddler are susceptible to exposure from chemicals in solid food (e.g. pesticides) and air (e.g. particulate matter) and through dermal exposure (e.g. heavy metals in soil). As children are introduced to day care and schools, potential new sources of exposure to certain chemicals (e.g. cleaning agents) may occur. Older children continue to be exposed to chemicals present in... 

Managing pediatric victims of chemical terrorism is an especially difficult challenge. In addition to the obvious physiologic and anatomic differences compared to adults (Table 61.1), there are important psychological and behavioral differences that put children at risk (Rotenberg and Newmark, 2003). Anecdotal reports have claimed that children are likely to be the first to manifest symptoms, to develop more severe manifestations, and to be hospitalized for other related illnesses. In fact, it is anticipated that children will be overrepresented among the initial index cases in a mass civilian exposure to toxic chemicals. Children have many characteristics that make them vulnerable to toxic exposures. The smaller mass of a child automatically reduces the dose of toxic agents needed to cause... 

Beyond the genetic factors, the causes of ADHD are unknown, and very few studies have examined the relationship between ADHD and exposures to environmental chemicals. It is known, however, that maternal prenatal exposures to lead, alcohol, tobacco smoke, and marijuana are known to result in the birth of children with high incidences of ADHD [14-17]. It has also been established that exposure to excessive quantities of phenylalanine either prenatally in utero, as a result of the mother having phenylketonuria (PKU) and fetus not having PKU, or postnatally where the child has PKU, results in the development of ADHD hyperactive and behavioral symptoms [18,19]. The mechanisms for these effects remain unknown, but these reactions to specific agents further demonstrate that environmental exposures may be triggers for ADHD. It is also known that many different chemicals trigger developmental... 

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