This extensive overview has addressed in a scientific manner the probable cause of autism. Although seemingly an impossible task, an important clue has always been autism’s triggered growth from the late 90s. This triggering eliminated genetics as a major cause and redirected it to changes in the anthropogenic environment. Global availability for ingestion by women of child-bearing years of all neurotoxic chemicals has been reviewed and potential changes examined. Surprisingly, these simple criteria eliminate almost everything except the neurotoxic metal elements. These are all present in recent blood analyses of pregnant women and also in the fetal cord with some at risk level concentrations. However, the two predominant neurotoxic elements that clearly stand out are Al and Hg. Furthermore, isotopically labeled experiments on animals coupled to fetal autopsies indicate that these in the forms of Al3+, HgCH3+ and HgC2H5+ can penetrate the usually tight blood/brain barrier and enter the brain with now known half-lives. Normally, these elements are controlled and neutralized by brain seleno-cysteine proteins. However, an overloading burden has become plausible in current times and even a temporary failure leaves the fetal brain vulnerable. For the first time, the burden is seen to arise not from a single source, but from the combination of medicine and diet. If these neurological illnesses are to be controlled, the body-burden for these and all the other toxins that the body has to constantly manage has to be reduced. To begin with, this will have to involve modifying currently high inoculation rates and procedures particularly in the US, and minimizing risks from consuming fish especially in a Japanese sushi life-style. This is not only of importance for women of child-bearing ages but for the whole population considering the consequences of such body burdens throughout life.


Autism; Triggered growth; Neurotoxins; Body-burden; Blood testing; Selenium importance; Multisource roles


Although it is the responsibility of the Environmental Protection Agency in the USA to assess environmental risks for its population, this is a major task, and they are faced with dozens of new chemical products each year. This is in addition to still having to reassess a backlog of hundreds of complex organic molecules that now show evidence of possible toxic natures and require re-examination to new standards [1]. Utilizing the analyses of urine samples from the US population in one large National Health and Nutrition Examination Survey a new methodology is in fact being suggested [2]. This is permitting approximate unknown levels of exposure to be modeled for general types of anthropogenic chemicals utilizing observed distributions of others in the main database. As a result, it is becoming a concern that this potential body-burden of undesired chemicals that have to be purged from the body and brain are possibly playing some role in the spectrum of neurological illnesses now seen in the aged and moreover also in the young. Although a demanding task, it is therefore appropriate to critically review the almost overwhelming number of publications that have appeared in recent years addressing this topic. The growth in analytical ability and its more widespread availability is an important advance, and now has spawned the acquisition of large medical databases of a more reliable nature. Moreover, more refined techniques of animal studies and isotopic labeling experiments have emerged. As a result, it is timely to pause and consider, in a more rigorous scientific manner, whether new insights are present particularly with emphasis on the current undeniable neurological epidemic evident particularly in the young. Although there is a rich literature on this subject and several excellent reviews, none have really examined the topic emphasizing the full chemical nature of the potential environmental species involved and how these have changed in recent decades in our diets.

Questions to be addressed in this environmental and neurotoxic review include:

• Which neurotoxins are most likely to have suddenly triggered an increase in autism cases starting in the 1990s? Can it be one, several or a synergist effect of toxins and neurotoxins? What has changed to have caused this on a globally distributed scale?

• How are these neurotoxins ingested?

• Why are babies and infants most affected?

• Are known toxic thresholds for chemicals adequately assessed and are “safe exposure levels” meaningful and at what degree of risk?

• Can the potential toxins in the body be adequately monitored by simple biomarkers and are these reasonably scaled to the prescribed ingestion rate or “safe exposure levels”?

• Do we have an approximate understanding of a neurotoxin’s destructive mechanisms?

• Are genetic susceptibilities involved or do DNA analyses simply reflect the consequence of toxic damage from some breakdown in the natural body defenses?

• Can this situation be changed by modifying the human environment or life-style?

• Does this apply mainly to births and pregnancies or are there neurological implications across the total population?

• As with smoking and drinking, should we accept a greater personal responsibility with the aid of modern medical testing for the state of our bodies?

• Should youngsters from birth through child-bearing years have their baseline body toxic-level summation be measured periodically?

Environmental Impacts on Humans

At present, society is plagued by various medical epidemics that appear to have a strong environmental basis. The current review examines one such situation in an attempt to see if sufficient information yet exists to pinpoint a potential cause and remedy. From about the year 2000, a new phrase has come into existence in medical diagnostics, namely “on the spectrum”. It relates to the now much larger and growing fraction of young children that exhibit neurological problems spanning a wide range of symptoms, but all a reflection of some DNA permanent brain damage. The most obvious and severe cases are termed autistic, which also displays their own spectral range of behavioral difficulties. This human defect now has been labeled for almost a century but generally was always at a very low incidence rate. However, as indicated in Figure 1, this has drastically changed within a very short period of about two decades, being most pronounced in the US. Although psychiatrics quibble about the diagnostic boundaries for autism there is no diminishing the overall magnitude of the problem however approximate the data may be. Teachers in schools can be the best measure of whether there has been change. Moreover, it is also reflected by the current need to establish specific schools, research and care centers in many communities. Such a growth rate that is also evident globally, but at a slightly lower rate in other countries is a very important piece of scientific data as it pinpoints a “triggering effect” that occurred in the later 1990 s and was not present at that rate before. Also, autism appears to show no racial, ethnic or social boundaries and does not relate readily to income, lifestyle or educational level [3].

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