Adverse pregnancy outcome in a petrochemical polluted area in Taiwan.

The petrochemical industry is the main source of industrial air pollution in Taiwan. Reported here are the results from an ongoing study of outdoor air pollution and the health of individuals living in a community in close proximity to petrochemical industrial complexes. The prevalences of term low birth weight (LBW) in the petrochemical municipality and control municipality were 3.22%, and 1.84%, respectively. After controlling for several possible confounders (including maternal age, season, marital status, maternal education, and infant sex), the adjusted odds ratio was 1.767 (1.002-3.116) for term LBW in the petrochemical municipality. Data provide further support for the hypothesis that air pollution can affect the outcome of pregnancy.

Increased risk of preterm delivery in areas with air pollution from a petroleum refinery plant in Taiwan.

The petrochemical and petroleum industries are among the main sources of industrial air pollution in Taiwan. Data in this study concern outdoor air pollution and the health of individuals living in communities in close proximity to a petroleum refinery plant. The prevalence of delivery of preterm birth infants was significantly higher in mothers living in a petroleum refinery area compared to controls in Taiwan. After controlling for several possible confounders (including maternal age, season, marital status, maternal education, and infant sex), the adjusted odds ratio was 1.41 (95% CI = 1.08-1.82) for delivery of preterm infants in the polluted region. Data support the view that air pollution can affect the outcome of pregnancy.

Female lung cancer mortality and sex ratios at birth near a petroleum refinery plant.

This study was conducted to assess whether female mortality from lung cancer is associated with residence in communities adjacent to a petroleum refinery plant and whether petroleum air pollution could affect the sex ratios of births. The Kaohsiung Refinery of the Chinese Petroleum Corp. is the oldest oil refinery in Taiwan and is located between the Tso-Ying and the Nan-Tzu municipalities. Standardized mortality ratios (SMRs) for female lung cancer and sex ratios of births were calculated for each municipality for the years 1971-1996. Cumulative-sum techniques were used to detect the occurrence of changes in the SMRs. The study results show that mortality from female lung cancer rose gradually about 30 to 37 years after the operation of a petroleum refinery plant began. However, the association between exposure to the petroleum air pollution and abnormal sex ratios at birth was not significant.

The facilitatory effect of N-methyl-D-aspartate on sexual receptivity in female rats through GnRH release.

The purpose of this study was to examine whether N-methyl-D-aspartate affects the sexual receptivity of female rats. Monosodium L-glutamate was used as a neurotoxin to induce hypogonadal status. Matured normal and monosodium L-glutamate-treated rats were ovariectomized and implanted subcutaneously with estradiol capsules. One week later, lordosis responsiveness was observed before and 10 min after N-methyl-D-aspartate (40 mg/kg of BW, ip) administration. The results showed that N-methyl-D-aspartate caused a remarkable increase of lordosis quotient in control rats but not in monosodium L-glutamate-treated rats. Moreover, the possible action site of N-methyl-D-aspartate in the enhancement of receptivity was evaluated by the post-castrational LH rise, pituitary LH release in response to GnRH, and N-methyl-D-aspartate-evoked GnRH releasability. The results revealed that: (a) serum levels of LH in monosodium L-glutamate-treated rats were lower (p < 0.01) than those of control rats after ovariectomy; (b) there was no significant difference of pituitary LH release responsiveness to GnRH test between two groups; and (c) N-methyl-D-aspartate-evoked LH release in monosodium L-glutamate-treated rats was similar to that in the control rats. In conclusion, N-methyl-D-aspartate may facilitate the sexual receptivity through stimulating GnRH release. The failure of N-methyl-D-aspartate in enhancing receptivity in monosodium L-glutamate-treated rats is probably due to the cellular damage by monosodium L-glutamate on specific areas responsible for lordosis.