"By equatiing it with DDT you downgrade it - unless you can show that DDT has the effects as described above."

Its all here Christmas all you had to do was Google "DDT" - and remember the use of this stuff was much more wider spread in time and area than Agent Orange ever was and that whereas Agent Orange has not been used for 40 years this stuff is still used widely today.

Effects on human health

Potential mechanisms of action on humans are genotoxicity and endocrine disruption. DDT may be directly genotoxic, but may also induce enzymes to produce other genotoxic intermediates and DNA adducts. It is an endocrine disruptor; The DDT metabolite DDE acts as an antiandrogen (but not as an estrogen). p,p'-DDT, DDT's main component, has little or no androgenic or estrogenic activity. Minor component o,p'-DDT has weak estrogenic activity.

Acute toxicity
DDT is classified as "moderately toxic" by the United States National Toxicology Program (NTP) and "moderately hazardous" by the World Health Organization (WHO), based on the rat oral LD50 of 113 mg/kg. DDT has on rare occasions been administered orally as a treatment for barbiturate poisoning.

Chronic toxicity

Diabetes
DDT and DDE have been linked to diabetes. A number of studies from the US, Canada, and Sweden have found that the prevalence of the disease in a population increases with serum DDT or DDE levels.

Developmental toxicity
DDT and DDE, like other organochlorines, have been shown to have xenoestrogenic activity, meaning they are chemically similar enough to estrogens to trigger hormonal responses in animals. This endocrine disrupting activity has been observed in mice and rat toxicological studies, and available epidemiological evidence indicates that these effects may be occurring in humans as a result of DDT exposure. The US Environmental Protection Agency states that DDT exposure damages the reproductive system and reduces reproductive success. These effects may cause developmental and reproductive toxicity:

- A review article in The Lancet states, "research has shown that exposure to DDT at amounts that would be needed in malaria control might cause preterm birth and early weaning ... toxicological evidence shows endocrine-disrupting properties; human data also indicate possible disruption in semen quality, menstruation, gestational length, and duration of lactation."

- Human epidemiological studies suggest that exposure is a risk factor for premature birth and low birth weight, and may harm a mother's ability to breast feed. Some 21st century researchers argue that these effects may increase infant deaths, offsetting any anti-malarial benefits. A 2008 study, however, failed to confirm the association between exposure and difficulty breastfeeding.

- Several recent studies demonstrate a link between in utero exposure to DDT or DDE and developmental neurotoxicity in humans. For example, a 2006 University of California, Berkeley study suggests that children exposed while in the womb have a greater chance of development problems, and other studies have found that even low levels of DDT or DDE in umbilical cord serum at birth are associated with decreased attention at infancy and decreased cognitive skills at 4 years of age. Similarly, Mexican researchers have linked first trimester DDE exposure to retarded psychomotor development.

- Other studies document decreases in semen quality among men with high exposures (generally from IRS).

- Studies generally find that high blood DDT or DDE levels do not increase time to pregnancy (TTP.) There is some evidence that the daughters of highly exposed women may have more difficulty getting pregnant (i.e. increased TTP).

- DDT is associated with early pregnancy loss, a type of miscarriage. A prospective cohort study of Chinese textile workers found "a positive, monotonic, exposure-response association between preconception serum total DDT and the risk of subsequent early pregnancy losses." The median serum DDE level of study group was lower than that typically observed in women living in homes sprayed with DDT.

- A Japanese study of congenital hypothyroidism concluded that in utero DDT exposure may affect thyroid hormone levels and "play an important role in the incidence and/or causation of cretinism."[69] Other studies have also found the DDT or DDE interfere with proper thyroid function.

Other
Occupational exposure in agriculture and malaria control has been linked to neurological problems (i.e. Parkinsons) and asthma.

Carcinogenicity
DDT is suspected to cause cancer. The NTP classifies it as "reasonably anticipated to be a carcinogen," the International Agency for Research on Cancer classifies it as a "possible" human carcinogen, and the EPA classifies DDT, DDE, and DDD as class B2 "probable" carcinogens. These evaluations are based mainly on the results of animal studies.
There is evidence from epidemiological studies (i.e. studies in human populations) that indicates that DDT causes cancers of the liver, pancreas and breast. There is mixed evidence that it contributes to leukemia, lymphoma and testicular cancer. Other epidemiological studies suggest that DDT/DDE does not cause multiple myeloma, or cancers of the prostate, endometrium, rectum, lung, bladder, or stomach.

Breast cancer
The question of whether DDT or DDE are risk factors of breast cancer has been repeatedly studied. While individual studies conflict, the most recent reviews of all the evidence conclude that pre-puberty exposure increases the risk of subsequent breast cancer. Until recently, almost all studies measured DDT or DDE blood levels at the time of breast cancer diagnosis or after. This study design has been criticized, since the levels at diagnosis do not necessarily correspond to levels when the cancer started. Taken as a whole such studies "do not support the hypothesis that exposure to DDT is an important risk factor for breast cancer." The studies of this design have been extensively reviewed.

In contrast, a study published in 2007 strongly associated early exposure (the p,p'- isomer) and breast cancer later in life. Unlike previous studies, this prospective cohort study collected blood samples from young mothers in the 1960s while DDT was still in use, and their breast cancer status was then monitored over the years. In addition to suggesting that the p,p'- isomer is the more significant risk factor, the study also suggests that the timing of exposure is critical. For the subset of women born more than 14 years before agricultural use, there was no association between DDT and breast cancer. However, for younger women—exposed earlier in life—the third who were exposed most to p,p'-DDT had a fivefold increase in breast cancer incidence over the least exposed third, after correcting for the protective effect of o,p'-DDT. These results are supported by animal studies.