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Part 3:

Environmental chemicals that provoke oxidative stress could contribute to autism or other health problems

During a typical day children and pregnant women are exposed to many different types of environmental chemicals that cause oxidative stress. These exposures add up, creating special concerns for infants and small children due to age-related sensitivity that derives from naturally low glutathione levels. This natural age-related vulnerability is exacerbated in individuals with impaired glutathione ratios. If these children were exposed to a high dose of any compound that produced significant oxidative stress, they would be less able to detoxify and excrete the compound.

Pervasive environmental contaminants like air pollutants from power plants and auto exhaust, pesticides, heavy metals and food additives all produce some degree of oxidative stress. Fine particulate matter and diesel exhaust both provoke tremendous oxidative stress and deplete glutathione (Li 2002). Oxygen radicals wreak havoc in the lungs of asthmatic children. The pain reliever acetaminophen and alcohol both provoke oxidative stress, but their combined effects are much more potent than either chemical alone.

Exposure to the pesticides maneb and paraquat can push neuron cells already under oxidative stress over a threshold of toxicity and "act as an additional insult to the system and prevent the normal recovery of [antioxidant] defenses" (Barlow 2005). Researchers have concluded that maneb disruptions to cells might cause neurodegeneration "especially with concurrent exposures to other environmentally relevant oxidative stressors, such as paraquat" (Barlow 2005). When they dosed pregnant mice with these pesticides the male offspring showed permanent alterations to neurological systems and enhanced susceptibility as an adult to paraquat (Barlow 2004).

PCBs induce a concentration-dependent increase in oxygen radicals. Cells with low levels of available glutathione are more sensitive to PCBs while cells pre-treated with antioxidants had reduced radical production and less cell death (Lee 2004).

Heavy metals—mercury, cadmium, chromium, cobalt, lead, antimony, nickel and others—are a major source of oxidative stress that are commonly detected in air, soil, water and food. Arsenic and chromium in pressure-treated wood, mercury in fish and vaccines, lead in paint, and metals in soil or drinking water are chronic if not daily sources of oxidative stress in the child's environment.

Glutathione is one of the bodys most important mechanism of heavy metal detoxification and excretion. Some metals—copper, chromium, iron and vanadium—directly provoke oxygen radical formation. Glutathione binds with these compounds as well as other metals—cadmium, lead, mercury, and nickel (Stohs 1995). The resulting, water-soluble chemical is more easily filtered out of the body. People with less 'active glutathione' will not be able to excrete metals as quickly. For example, cells treated with chemicals to inhibit glutathione recycling are much more sensitive to manganese toxicity (Desole 1997). People chronically exposed to arsenic in drinking water have increased oxidative damage and decreased antioxidant potential (Wu 2001).

Numerous studies link thimerosal with oxidative stress to the brain and neurological system at concentrations similar to those that were experienced by children vaccinated in the 1990s. Researchers measured mercury concentrations between 10 and 30 nanomoles per liter (nM) in premature infants given a single Hepatitis B shot at birth (Stajich 2000). Mercury concentrations ranging from 4 to 21 nM are reported in young children when measurements were collected 3 to 20 days after vaccination (Pichichero 2002). Four recent studies of thimerosal toxicity to human brain cells report oxidative damage, interruption of methylation, and decreased cell energy resulting from thimerosal exposure in the range of exposure overlapping with those for vaccinated children in the 1990s (Waly 2004, Baskin 2003, Ueha-Ishibashi 2004, Makani 2002). Several studies documented the protective benefits of antioxidants, especially glutathione, which attenuate the damages caused by thimerosal (Makani 2004, James 2005, Shanker 2003).

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