Potential biologic mechanisms behind this association may involve an effect of air pollution on the placenta, embryo, maternal immunologic system, ovarian–hypothalamic axis, and the induction of IUGR, which can lead to a more vulnerable fetus. It is possible that certain toxics emitted in motor vehicle exhaust, such as polycyclic aromatic hydrocarbons (PAHs), may be responsible for these adverse birth outcomes. Exposure to PAHs during pregnancy has been demonstrated to alter levels of serum progesterone and estrogens, decrease survival of rats, and relate to endocrine disorders in rodents (Takeda et al. 2004). Air particles may be associated with changes in plasma viscosity (Peters et al. 1997), inflammatory process (Dubowsky et al. 2006), and elevation in blood pressure in susceptible populations (Brook 2005). Carbon monoxide easily crosses the placental barrier, coming into contact with the fetus, leading to a rapid accumulation of carboxyhemoglobin, with subsequent reduction in oxygen transportation by blood (Aleixo Neto 1990).