The aims of this study were to evaluate whether air pollution during pre-natal and post-natal phases change habituation and short-term discriminative memories and if oxidants are involved in this process. As secondary objectives, it was to evaluate if the change of filtered to nonfiltered environment could protect the cortex of rats against oxidative stress as well as to modify the behavior of these animals. Wistar, male rats were divided into four groups (n = 12/group): pre and post-natal exposure until adulthood to filtered air (FA); pre-natal period to nonfiltered air (NFA-FA); until (21st post-natal day) and post-natal to filtered air until adulthood (PND21); pre-natal to filtered air until PND21 and post-natal to nonfiltered air until adulthood (FA-NFA); pre and post-natal to nonfiltered air (NFA). After 150 days of air pollution exposure, animals were tested in the spontaneous object recognition test to evaluate short-term discriminative and habituation memories. Rats were euthanized; blood was collected for metal determination; cortex dissected for oxidative stress evaluation. There was a significant increase in malondialdehyde (MDA) levels in the NFA group when compared to other groups (FA: 1.730 +/- 0.217; NFA-FA: 1.101 +/- 0.217; FA-NFA: 1.014 +/- 0.300; NFA: 5.978 +/- 1.920 nmol MDA/mg total proteins; p = 0.007). NFA group presented a significant decrease in short-term discriminative (FA: 0.603 +/- 0.106; NFA-FA: 0.669 +/- 0.0666; FA-NFA: 0.374 +/- 0.178; NFA: -0.00631 +/- 0.106 sec; p = 0.006) and an improvement in habituation memories when compared to other groups. Therefore, exposure to air pollution during both those periods impairs short-term discriminative memory and cortical oxidative stress may mediate this process.

Exposure to air pollution can elicit cardiovascular health effects. Children and unborn fetuses appear to be particularly vulnerable. However, the mechanisms involved in cardiovascular damage are poorly understood. It has been suggested that the oxidative stress generated by air pollution exposure triggers tissue injury. To investigate whether prenatal exposure can enhance oxidative stress in myocardium of adult animals, mice were placed in a clean chamber (CC, filtered urban air) and in a polluted chamber (PC, São Paulo city) during the gestational period and/or for 3 mo after birth, according to 4 protocols: control group-prenatal and postnatal life in CC; prenatal group-prenatal in PC and postnatal life in CC; postnatal group-prenatal in CC and postnatal life in PC; and pre-post group-prenatal and postnatal life in PC. As an indicator of oxidative stress, levels of lipid peroxidation in hearts were measured by malondialdehyde (MDA) quantification and by quantification of the myocardial immunoreactivity for 15-F2t-isoprostane. Ultrastructural studies were performed to detect cellular alterations related to oxidative stress. Concentration of MDA was significantly increased in postnatal (2.45 +/- 0.84 nmol/mg) and pre-post groups (3.84 +/- 1.39 nmol/mg) compared to the control group (0.31 +/- 0.10 nmol/mg) (p < .01). MDA values in the pre-post group were significantly increased compared to the prenatal group (0.71 +/- 0.15 nmol/mg) (p = .017). Myocardial isoprostane area fraction in the pre-post group was increased compared to other groups (p < or = .01). Results show that ambient levels of air pollution elicit cardiac oxidative stress in adult mice, and that gestational exposure may enhance this effect.

The cerebellum and hippocampus seem to be more susceptible than other brain structures to in vitro direct PM exposure assay and the oxidative stress pathway catalyzes the neurotoxic effect of PM exposure, as evidenced by high consumption of CAT and high levels of TBA-RS. Thus, PM direct exposure seems to activate toxic neurological effects.

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Epidemiological studies have demonstrated the adverse effects of particulate matter (PM) inhalation on the respiratory and cardiovascular systems. It has been reported that air pollution may affect the central nervous system and decrease cognitive function. In rats, residual oil fly ash (ROFA) instillation causes decreased motor activity and increased lipid peroxidation in the striatum and the cerebellum. Our objective was to determine whether chronic instillation of particles induces changes in learning and memory in rats and whether oxidants in the hippocampus may contribute to these adverse effects. Forty-five-day-old male Wistar rats were exposed to ROFA by intranasal instillation and were treated with N-acetylcysteine (NAC) at 150 mg/kg i.p. for 30 days. Control groups were exposed to ROFA, NAC, or neither. On days 1, 8, and 30 of the protocol, rats were submitted to the open field test to evaluate habituation. After the last open field session, the rats were killed by decapitation. The hippocampus was used to determine lipid peroxidation (LP) by the thiobarbituric acid-reactive substances test. ROFA instillation induced an increase in LP in the hippocampus compared to all treatment groups (p = .012). NAC treatment blocked these changes. All of the treatment groups presented a decrease in the frequency of peripheral walking (p = .001), rearing (p = .001), and exploration (p = .001) over time. Our study demonstrates that exposure to particles for 30 days and/or NAC treatment do not modify habituation to an open field, a simple form of learning and memory in rats, and that oxidative damage induced by ROFA does not modulate these processes.

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The air pollution is a public health problem. The pregnancy period is critical because mother's exposure to air pollutants could affect the fetal development of humans and animals.Studies in animals and humans had demonstrated the association between the mother's exposure to air pollutants, neonatal mortality and birth defects [1][2][3][4]. Veras et al. [3] demonstrated an increase in transplacental diffusion of substances in female mouse which were exposed to air pollution at ambient level during the pre-pregnancy and pregnancy periods. In 2009 [4], the same researchers showed that females which inhaled PM (particulate matter) at ambient level presented a decrease in the number of cicles, of folicules and embryo implantation as well as lower weight of puppies. Reliene et al. [5] showed an increase in frequency of mutations in DNA (desoxiribonucleic acid) of puppies whose mothers were exposed to PM.In studies with women, Lacasãna et al. [6] revealed an association between the increment of 10 µg/m 3 in concentration of PM 10 and 22% in the deaths of neonates by respiratory diseases. The maternal exposure to O 3 in the second and to CO in third month of pregnancy caused a loss in weight of babies [7][8][9][10]. Moreover, the pregnant women who inhaled NO 2 during gestational period present an increase of 25% premature delivery [11]. The mechanism that was suggested to clarify the association between CO and the low weight of neonates would be the competition between this gas and O 2 for the sites in hemoglobin, which would decrease the transport of O 2 to the tissues and harm the fetal development. In terms of the association between O 3 and the decrease in neonate weight, animal studies suggested that this effect would be modulated by maternal inflammatory process. The prematurity could be explained through oxidation of proteins and lipids by NO 2 and the decrease of antioxidant protection of fetus and mother. Experimental studies demonstrated that inhalation of NO 2 during gestational period induced the oxidation of lipids, which are components of placenta, and increased the lethality in post-implatantion period of embryo [12]. Gilboa et al. [13] showed the existence of a positive association between the exposure to CO and the Fallot Tetrology (odds ratio: 2,04); between PM 10 and atrial septus defects (odds ratio: 2,27) and between SO 2 and ventricular septus defects (odds ratio: 2,16). Ritz et al. [14] found CO and O 3 inhaled during the second month of pregnancy, which is a critical period for heart development, caused congenital cardiac malformation.Considering the studies which were presented in this editorial, the mechanisms that are involved in injuries caused to air pollution in pre and post-natal periods are not well known. Therefore, there is a necessity to study more and to increase our knowledge about this subject to determine the effects of pollutant inhalation during the gestational period in adult age. Moreover, these kinds of studies are important to create public health policies to decrease the...