The strongest negative correlations for the pollutant levels were those that were six months apart, e.g., months one vs. late gestation were associated with decreases in CD3+and CD4+fractions and increases in CD19+and NK cell fractions. There was no significant association between alterations in lymphocyte distribution and air pollution exposure during the mid gestation. == Conclusions == PAHs and PM2.5in ambient air may influence fetal immune development via shifts in cord blood lymphocytes distributions. Associations appear to differ by exposure in early versus late gestation. == Introduction == Ambient air pollution can affect child [1] and perinatal health [2,3]. Exposures to environmental toxicants during early life are of particular concern because developing organ systems may be especially susceptible to low-dose insults, as compared with adult life [4]. As a result, early-life exposures are more likely to produce persistent adverse outcomes [5]. However, mechanisms for such effects are less clear. It has been suggested that some aspects of air pollutant toxicity may be mediated through effects on the immune system [6]. T and B cell development start during the earlier weeks of gestation [7]. There is growing evidence that exposure Rabbit polyclonal to ADCY2 to immunotoxic compounds may not only cause immuno-suppression but also result in increased expression of aberrant immune responses. A report from Cetylpyridinium Chloride a workshop to identify critical windows of exposure suggests three critical phases of immune development: (1) weeks eight – 10: initiation of hematopoiesis, (2) weeks 10 – 16: hematopoietic cell migration and progenitor cell expansion and (3) weeks 16 – birth: colonization of bone marrow and thymus [8]. Toxic exposure during early gestation could result in failure of stem cell formation or abnormal formation whereas exposure in the later phases may interrupt cell migration [9] and subsequent proliferation [10]. Animals models also support the presence of differential windows of vulnerability in relation to toxicants such as lead [11]. As part of a larger investigation of the effects of air Cetylpyridinium Chloride pollution on fetal and child health and development in the Czech Republic, we reported earlier that exposures to polycyclic aromatic hydrocarbons (PAH) and fine particles (< 2.5 microns, PM2.5) in ambient air during the 14 days prior to birth were associated with a decrease in the percentage of T lymphocytes and an increase in the percentage of B lymphocytes in cord blood [12]. We also found that greater chronic exposure to air pollution resulted in higher NK cell fractions in cord blood of newborns [13]. This report extends those findings by focusing on timing of exposures to air pollution throughout gestation and the relationship to immune markers at birth. Given that lymphocyte production, including T and B cell development, starts early in gestation [7] and that critical stages in development of the immune system may also reflect temporal variation in susceptibility to immunotoxicants, this study investigated the association between maternal exposure to air pollution during each month of gestation and cord blood lymphocyte proportions. == Methods == The study was based in two districts of the Czech Republic, where fixed air pollution monitoring sites were established. One was in Teplice in Northern Bohemia, which is characterized by mining Cetylpyridinium Chloride operations and coal-fired power plants within an area of 479 km2; the other was located in Prachatice in Southern Bohemia, which has light industry within an area of 1375 km2. The populations in Teplice and Prachatice were about 120,000 and 50,000 respectively. == Subject enrollment and data collection == Women who delivered between May 1994 and March 1999 in the two.