Substances in Diesel Exhaust Listed by Cal EPA as Toxic Air Contaminants many of which are endocrine disruptors
Nobue Watanabe and Masayuki Kurita
Department of Environmental Health, Tokyo Metropolitan Research Laboratory of Public Health, Tokyo, Japan
Abstract
This study was conducted to determine the impact of diesel exhaust inhalation on
the fetus. Seventy-two pregnant rats and 18 nonpregnant rats were divided into
three groups: a group exposed to total diesel engine exhaust containing 5.63
mg/m3 particulate matter, 4.10 ppm nitrogen dioxide, and 8.10 ppm
nitrogen oxide; a group exposed to filtered exhaust without particulate matter;
and a group exposed to clean air. The exposure period was from day 7 until day
20 of pregnancy. In addition, 15 pregnant rats were treated with aromatase
inhibitors or testosterone to clarify the process by which diesel exhaust exerts
its toxicity. The anogenital distance was significantly longer in male and
female fetuses from both exhaust-exposed groups than in those of the control.
Differentiation of the testis, ovary, and thymus was delayed and disturbed.
Maternal testosterone and progesterone levels, which increased due to pregnancy
whether or not the rats were exposed, were significantly higher and lower,
respectively, in the pregnant rats exposed to total exhaust and filtered
exhaust. The serum adrenocorticotropic hormone (ACTH) level and urinary
excretion of 17-hydroxycorticosteroids (OHCS) did not differ among the pregnant
groups. These results indicate that elevated testosterone did not result from
elevated maternal adrenal function. The feto-placental-ovarian unit and
inhibition of aromatase activity and synthesis caused by diesel exhaust
inhalation might have played an essential role in the accumulation of
testosterone. Since both exhaust-exposed groups showed almost the same reactions
toward the inhalation, the gaseous phase must have included the relevant
toxicants. Key words: diesel exhaust, feto-placental-ovarian unit, fetus,
masculinization, ovary, pregnancy, rats, testis, testosterone, thymus. Environ
Health Perspect 109:111-119 (2001). [Online 11 January 2001]
http://ehpnet1.niehs.nih.gov/docs/2001/109p111-119watanabe/abstract.html
Address correspondence to N. Watanabe, Department of Environmental Health, Tokyo Metropolitan Research Laboratory of Public Health, 24-1 Hyakunincho 3 chome, shinjuku-ku, Tokyo 169-0073, Japan. Telephone: (81) 3-3363-3231. Fax: (81) 3-3368-4060. E-mail: nobuew@tokyo-eiken.go.jpReceived 7 July 2000; accepted 22 August 2000
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