Project at a Glance

Title: Studies of young adult female responses to acute ozone exposure

Principal Investigator / Author(s): Adams, William C

Contractor: UC Davis

Contract Number: A933-096 & A033-176

Topic Areas: Health Effects of Air Pollution


The primary purposes of this research were to determine if: (1) young adult females respond with greater acute effects of ozone (O3) than their mate counterparts at a dose relative to lung size as well as at the same total dose; (2) O3 response in females is influenced by the disparate levels of progesterone (a steroid hormone) that they experience during the various phases of their menstrual cycles; and (3) O3 exposure has an effect on the integrity of normal menstrual cycles of healthy young adult females.

In the first study, twenty healthy young adult males and females were exposed to Filtered air (FA), 0.18 parts per million (ppm) and 0.30 ppm O3 via an obligatory mouthpiece inhalation system for 60 minutes while exercising continuously on a bicycle ergometer at work rates set to elicit an average minute ventilation of 50 1/min for female subjects and 50 and 70 1/min for male subjects. The twenty females were exposed to each gas mixture during three phases of their menstrual cycle: the early follicular (EF) (low progesterone), the mid-luteal (ML) (high progesterone) and late luteal (LL) (decreasing progesterone), In the second study, an additional eleven females were exposed in similar fashion to 0.30 ppm 03 and to FA during the EF and ML phases of their menstrual cycles. Experimental effects were determined via pre- and post-exposure standard pulmonary function and subjective symptom measurements, while values for exercise ventilation and respiratory metabolism were monitored periodically during exposures. Analysis of daily urine samples provided documentation of normal menstrual cycles as well as the concentrations of progesterone during the cycle phases.

In the first study, responses of female subjects were compared to those of male subjects following an 03 dose that was similar (ventilation for males and females = 50 l/min), as well as one that corrected for gender differences in lung size and / or maximal oxygen uptake (i.e., female = 50 l/min and male = 70 1/min). Although the female's responses were intermediate to those observed for the male's two exposures, no significant differences between the groups' pulmonary function and subjective symptoms of respiratory discomfort were found for either the same absolute dose or relative dose exposures to 0.18 ppm and 0.30 ppm O3. When exposed to O3 during various assumed phases of their menstrual cycle, the female group did not respond differentially as reflected by the values obtained for pulmonary function parameters: forced vital capacity (FVC); forced expiratory volume in is (FEVl.0) and forced expiratory flow between 25-75 percent of forced vital capacity (FEF25-75). However, merged data from the two studies utilizing a total of 13 females with normal menstrual cycles (i.e., with respect to maintenance of intact phases at least up to the point of each exposure), revealed a nonsignificant (P < O. 12) trend towards greater FEVl.0 impairment during the EF phase (when progesterone levels were low) compared to the ML phase when progesterone was significantly higher. It was suggested that the pronounced difference in progesterone levels during the EF and ML phases of the menstrual cycle could be responsible for the FEVI.O difference via its steroidal effect (anti-inflammatory) on known O3-induced respiratory tract inflammation, which has been shown by others to be related to pulmonary function impairment.

A significant number of females experienced menstrual cycle disruptions following exposure to 0.30 ppm O3 as evidenced by delays in ovulation, shortened luteal phases and secondary surges in estrogen during the lace luteal phase. These disturbances are most likely not attributable to changes in diet, stress or activity levels. The mechanism by which 03 interferes with normal ovarian functioning is unknown at this time, but appears to be focused at the pituitary (rather than the ovaries), since lutenizing hormone, the hormonal signal for ovulation, also appears to be affected by O3 exposure. Although these effects seem to be temporary (lasting 1 or 2 cycles), the reproductive viability of the females involved was clearly compromised during those cycles. It was suggested that further research be done in this area to determine the implications of this previously unreported observation.

For questions regarding this research project, including available data and progress status, contact: Research Division staff at (916) 445-0753

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