A study published in the journal Toxicological Sciences found that exposure to the common environmental pollutant 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) increased the risk of lower urinary tract symptoms (LUTS) related to benign prostatic hyperplasia (BPH) in genetically susceptible mice.
TCDD, often referred to simply as dioxin, is one of the most widely spread environmental toxins. It is present in drinking water and, according to the U.S. Environmental Protection Agency, stems in large part from backyard burning of waste as well as from manufacturing and refining processes. The
chemical is highly toxic and only slowly eliminated from the body, so
that exposure to even the low amounts found in the environment are
potentially dangerous for human health. The half-life of TCDD in humans
is 7–11 years, and experimental animals exposed to higher levels have a
delayed or incomplete prostate development. The chemical also increases
cancer risk.
Evidence for a fetal origin of prostatic disease is beginning to
emerge. To test whether genetically susceptible mice would develop more
severe LUTS following TCDD exposure, University of Wisconsin
researchers used a mouse with mutations predisposing it to prostate
hyperplasia. Pregnant mice received one single dose of TCDD that was low
enough not to cause a disruption in prostate development, but high
enough to remain in the mice pups throughout weaning.
When male mice were adult, some were also exposed to higher levels of
testosterone and estradiol in doses that are known to cause urinary
disturbance in mice, and were then allowed to live for four more months.
According to the report — titled “In utero and Lactational TCDD Exposure Increases Susceptibility to Lower Urinary Tract Dysfunction in Adulthood“ — the
mice that were exposed to TCDD alone had a reduced voiding pressure.
Otherwise, TCDD exposure had little effect on the lower urinary
tract anatomy or function.
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