Joint effect of particulate matter and cigarette smoke on women's sex hormones.

BACKGROUND: Although relationships between exposure to air pollution and reproductive health are broadly studied, mechanisms behind these phenomena are still unknown. The aim of the study was to assess whether exposure to particulate matter (PM10) and tobacco smoking have an impact on menstrual profiles of 17ß-estradiol (E2) and progesterone (P) and the E2/P ratio. METHODS: Levels of sex hormones were measured daily in saliva during the entire menstrual cycle among 132 healthy, urban women. Exposure to smoking (active or passive) was assessed by questionnaire, whilst exposure to PM10 with municipal monitoring data. RESULTS: During the early luteal phase, profiles of E2 were elevated among women with higher versus lower exposure to PM10 (p = 0.02, post-hoc tests). Among those who were exposed versus unexposed to tobacco smoking, the levels of mean E2 measured during the entire cycle were higher (p = 0.02). The difference in mean E2 levels between the group of joint exposure (i.e. to high PM10 and passive or active smoking) versus the reference group (low PM10, no smoking) was statistically significant at p = 0.03 (18.4 vs. 12.4 pmol/l, respectively). The E2/P ratios were higher among women with higher versus lower exposure to PM10 and this difference was seen only in the early luteal phase (p = 0.01, exploratory post-hoc tests). CONCLUSIONS: We found that PM10 and tobacco smoking affect ovarian hormones independently and do not interact with each other. Both exposures appear to have estrogenic effects even though women's susceptibility to these effects differs across the menstrual cycle. We propose that the hormonal mechanisms are involved in observed relationships between air pollution and smoking with women's reproductive health.

Low estradiol levels in women of reproductive age having low sleep variation.

Higher exposure to light at night, for example, owing to night shift work or decrease in sleep duration, may suppress melatonin production, which in turn may increase the reproductive hormone levels. High levels of steroid hormones, especially estrogens, may be associated with an increase of the breast cancer risk. This study investigated whether variation in the sleep duration during one entire menstrual cycle corresponds to estradiol saliva concentrations in healthy, urban women of reproductive age. During 2000-2001, 95 regularly menstruating women aged 24-36 in Poland collected daily saliva samples for one entire menstrual cycle. Saliva samples were analyzed for concentration of 17-beta estradiol (E2) using radio immunoassay. Information on the number of hours of sleep per night (sleep duration) was collected daily by questionnaires for one entire menstrual cycle. Using covariance analysis, after adjustments for sleep duration, we documented a positive relationship between the sleep variation (sleep coefficient of variation) and E2 levels in women of reproductive age. Mean levels of E2 differed significantly in women from the lowest sleep coefficient of variation quartile (13.93 pmol/l) in comparison with other quartiles (22.35 pmol/l), (P<0.001). The low sleep variation group, that is, the women who sleep regularly, had mean E2 levels 60% lower than other groups. These results suggest that sleep variation significantly correlates with E2 levels, whereas sleep duration does not show a statistically significant relationship. This study suggests that sleep variation may influence endogenous estrogens, which is of importance for risk of breast cancer.