Background:Toxic volatile organic compounds (VOC), like benzene, toluene, ethylbenzene and xylenes (BTEX), are atmospheric pollutants representing a threat to human health. They are released into the environment from mobile sources in urban settings, but newly polluted areas are gaining importance in countries where accelerated industrialization is taking place in suburban or rural settings.Methods:The review includes studies done in Mexico and Latin-America and countries considered to have emerging economies and are compared with similar studies in developed countries. Data about environmental VOC levels and exposure of children have been included. Also, information about health effects was reviewed. Articles were searched in PubMed and Scopus, and information was also obtained from the United States Environmental Protection Agency (EPA), the EPAs Integrated Risk Information System (IRIS-EPA) and state reports on air quality of Mexican cities.Results:VOC or BTEX levels reported in industrial and suburban areas were found to be higher due to the burning of fossil fuels and waste emission; whereas, in big cities, VOC emissions were mainly due to mobile sources. Even though TEX levels were under reference values, benzene was found at levels several times over this value in cities and even higher in industrial zones. Elevated VOC emissions were also reported in cities with industrial development in their peripheral rural areas.Public health relevance:Industrial activities have changed the way of life of small towns, which previously had no concern about environmental pollution and chemicals. No air monitoring is done in these places where toxic chemicals are released into rivers and the atmosphere. This work demonstrates the need for environmental monitors to protect human life in suburban and rural areas where industrial growth occurs without planning and ecological or health protection, compromising the health of new generations beginning in fetal development.

Chromatin buds (CHB), broken eggs, or budding cell nuclei are structures similar to micronuclei (MN) in shape, structure, and size, which are linked to the main nuclei of cells by a thread or stalks of chromatin. They have been observed in numerous cell types and there are reports of their existence relating them with MN or with genotoxic events. However, there is no systematic study reporting their frequency and no experiment has been done to ascertain whether they are really induced by genotoxins. Furthermore, they have been discarded as genotoxic events with the argument that they are not formed in dividing cells. Studies are presented here that indicate that CHB can be considered as genotoxic events and that their origin is comparable to that of MN. Bromodeoxyuridine (BrdU) was used to label proliferating lymphocytes, which were later identified by means of an immunohistochemical method, using the H2O2-DAB stain. The results show that CHB are consistently formed where MN are seen. CHB were induced by the clastogen mitomycin C (MMC) as well as by the aneuploidogen colcemid, with frequencies similar to MN in both cases, and to multinucleated cells in the case of colcemid. CHB occur in lymphocytes of smokers with frequencies similar to those of MN, and we found that the infection with Taenia solium metacestodes induced a comparable increase of both MN and CHB frequency in lymphocytes from pigs.

Exposure to organochlorine pesticides was studied in a group of mother-infant pairs living in a rural area where agriculture is the main economic activity. Fumigation in this zone is performed with airplanes, thus affecting the inhabited areas around them, including schools. Heparinized venous blood of mothers and umbilical cords was used to evaluate the olive tail moment in the comet assay, and micronuclei, chromatin buds, and nucleoplasmic bridges in peripheral blood lymphocytes. Cord blood samples were taken at the moment of birth only from natural and normal parturitions. Determinations of hexachlorobenzene, aldrin, heptachlor epoxide, oxichlordane, t and c-chlordane, cis-nonachlor, mirex, alpha and beta-endosulfan, alpha, beta and gamma hexachlorocyclohexane, and p'p'-DDT, p'p'-DDE were conducted to establish the differential distribution of the toxicants between compartments, i.e., mother and umbilical cord. Significantly higher pesticide levels were found in umbilical cord plasma than in mothers' plasma for almost all compounds tested, except DDE and oxychlordane. Significantly higher olive tail moments were found in umbilical cords than in mothers, whereas micronuclei frequencies were higher in mothers than in umbilical cords. However, neither the levels of micronuclei nor the olive tail moment were correlated with pesticide levels. Given that no other exposure to toxic compounds has been identified in this region, the lack of correlation between genotoxicity biomarkers and pesticide levels may be due to the variability of the exposure and to endogenous processes related to lipid mobility during pregnancy, the metabolism of the compounds, and individual susceptibilities.

A study was realized to ascertain whether eight selected pesticides would induce double strand breaks (DSB) in lymphocyte cultures and whether this damage would induce greater levels of proteins Rad51 participating in homologous recombination or of p-Ku80 participating in nonhomologous end joining. Only five pesticides were found to induce DSB of which only glyphosate and paraoxon induced a significant increase of p-Ku80 protein, indicating that nonhomologous end joining recombinational DNA repair system would be activated. The type of gamma-H2AX foci observed was comparable to that induced by etoposide at similar concentrations. These results are of importance since these effects occurred at low concentrations in the micromolar range, in acute treatments to the cells. Effects over longer exposures in actual environmental settings are expected to produce cumulative damage if repeated events of recombination take place over time.

Even in socially monogamous species, sexual conflict is one reason that often promotes differences in the roles of sexes during reproduction, which may lead to one sex making a disproportionate contribution, and thus incurring disproportionate costs, at particular moments of the breeding process. In Mexico City, a number of songbird species line their nests with fibers from discarded cigarette butts, which reduce ectoparasite load but are genotoxic. As male Passer domesticus make substantial contributions to nest building whereas male Carpodacus mexicanus do not contribute to nest building, we hypothesized that the toxic effects of exposure to cigarette butts should be greater for females C. mexicanus than for conspecific males, but that there should be little or no difference in P. domesticus. As expected there was more exogenous genotoxic damage in the red-blood cells of incubating female C. mexicanus the more cigarette butts were found in their nest, and much more than in their conspecific males. Damage in males was not associated to cigarette butts; it was initially lower than in females, but it increased near fledging, together with their breeding effort. In both male and female P. domesticus, however, genotoxic damage was equally apparent and greater the more cigarette butts were in the nest. The novel use of a toxic, anthropogenic parasite repellent by urban birds may be thus asymmetrically increasing the breeding costs paid by the member of the pair most involved in nest building and incubation.