DIOXIN
Exposures during fetal development have been implicated in endocrine related cancers in women (breast and uterine, for example) by altering hormone levels, increasing the sensitivity of children and adolescents to other carcinogens (Birnbaum and Fenton 2003).
In men, tiny levels of dioxin in the range of 0.02-10 parts per billion (ppb) alter testosterone levels and are linked with diabetes (EPA 2004a). Dioxin at 80 parts per trillion in paternal – but not maternal – serum causes a significant change in the sex ratio of children (Mocarelli, et al. 1996, Mocarelli, et al. 2000). At this tiny dose, men father nearly twice as many girls as boys.
As body burdens increase within and above these ranges, the likelihood, severity, and potential spectrum of non-cancer effects increases (EPA 2004a).
Fetal dioxin exposure can harm the immune system, thyroid, and brain (Van Loveren et al. 2003, Faroon et al. 2001, Tusscher and Koppe 2004). Dioxin from garbage incinerators is associated with increased incidence of infant death and birth defects (Tango et al. 2004).
METHYL MERCURY
Exposure in the womb causes measurable declines in brain function in children exposed to levels corresponding to 58 ppb in maternal blood (NAS 2000b).
Researchers in the Netherlands found a doubling in the risk of heart attacks and death from coronary heart disease at methylmercury hair levels of 2 mg/kg, which corresponds to about 1/5 the assumed safe maternal blood level (Salonen, et al. 1995).
Increased diastolic and systolic blood pressure and decreased heart rate variability in developmentally exposed children have also been observed at doses below what the EPA considers a safe maternal blood level (NAS 2000b, Sorensen et al. 1999).
PCBs at 9.7 ppb in maternal serum during foetal development can impair brain development, with resultant attention and IQ deficits that appear to be permanent (Jacobson and Jacobson 1996).
Notably, IQ deficits are linked to the mother’s PCB levels, not the PCB levels in children at 4 and 11 years of age (by which time the children’s PCB levels had decreased substantially compared to levels at birth), underscoring the limitations of studies that look for correlations between current body burdens and health effects in the absence of data on in utero exposures.
Levels of PCBs in the general American population are also associated with abnormal menstrual cycles (Cooper et al. 2005).
DDE
Above 15 ppb in maternal blood is associated with pre-term birth and low birth weight, with weight corrected for gestational age (Longnecker et al. 2001). DDE is a metabolite of the banned, persistent pesticide DDT.
Using the associations derived from tests of archived blood samples from a pool of 42,000 women, researchers estimated that DDT exposures in the US population could have accounted for up to 15% of infant deaths during the 1960s.
Low birth weight is recognized as a risk factor for type II diabetes, high blood pressure, and cardiovascular disease later in life (Prentice and Moore 2005, Godfrey and Barker 2001, Hales and Barker 2001).
Even if these lower birth weight babies “catch up” later, the damage may have already been done. A substantial number of studies have found that low birth weight followed by an accelerated growth rate during childhood is a significant risk factor for high blood pressure, stroke, insulin resistance and glucose intolerance (Eriksson, et al. 2000a, Eriksson, et al. 2002, Eriksson et al. 2000b, Eriksson et al. 1999, Eriksson and Forsen 2002, Forsen et al. 2000, Ong and Dunger 2002, Stettler et al. 2002).
Over 300 chemicals are found in our bodies. Find out how you can reduce exposures in the CAP Guide, Contaminated Humans