LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades, Asunción, Paraguay.
ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4084.
DOI: https://doi.org/10.56712/latam.v5i4.2550
Oral epithelial cells of schoolchildren exposed to air
pollution may develop cytotoxic and genotoxic damage
Daños citotóxicos y genotóxicos en células epiteliales orales de escolares
expuestos a la contaminación atmosférica
Marco Antonio García Zarate
margarci@cicese.mx
https://orcid.org/0000-0003-3293-3000
Center for Scientific Research and Higher Education of Ensenada, B. C. Applied Physics Department
Ensenada Baja California México
María Evarista Arellano García
evarista.arellano@uabc.edu.mx
https://orcid.org/0000-0002-0997-6902
Autonomous University of Baja California, Science Faculty
Ensenada Baja California México
Zayre Ivonne González Acevedo
zgonzale@cicese.edu.mx
https://orcid.org/000-0003-3293-0563
Center for Scientific Research and Higher Education of Ensenada, B. C. Earth Science Division
Ensenada Baja California México
Olivia Torres Bugarín
olivia.torres@edu.uag.mx
https://orcid.org/0000-0003-4541
Universidad Autónoma de Guadalajara. Unidad Académica de Ciencias de la Salud, Facultad de Medicina
Guadalajara, Jalisco México
Artículo recibido: 12 de agosto de 2024. Aceptado para publicación: 26 de agosto de 2024.
Conflictos de Interés: Ninguno que declarar.
Abstract
As petrol stations emit pollutants into the atmosphere, their proximity to schools can affect air quality
both inside and outside classrooms. School-age children, who spend five to seven hours a day in
classrooms and playgrounds during the school year, may be at risk of inhaling potentially harmful
gases and particles, which could have a negative impact on their health and academic performance.
A biomonitoring study was carried out on 143 children from three schools. Two of the schools were
considered to be exposed to volatile organic compounds (VOCs) and were located 50 and 300 metres
away from petrol stations. The other school, which was not considered to be exposed, was located
450 metres away. With the exception of MN, the biomarkers of genotoxic damage were generally
higher (p>0.05) in the school located 50 metres from a petrol station than in the control group, although
the results were less clear in the school located 300 metres away. For all biomarkers (KR, CC, PN and
KL), the school 50 metres from the source of emissions had higher levels of cytotoxicity (p <0.05). This
is the first study to link exposure to volatile hydrocarbons in petrol to genotoxic damage in children,
and it strongly suggests that urban planning laws should be changed to halt the decline in children's
health.
Keywords: volatile organic compounds, micronuclei, nuclear abnormalities, gas stations, air
pollution
LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades, Asunción, Paraguay.
ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4085.
Resumen
Dado que las gasolineras emiten contaminantes a la atmósfera, su proximidad a las escuelas puede
afectar a la calidad del aire tanto dentro como fuera de las aulas. Los niños en edad escolar, que pasan
entre cinco y siete horas al a en aulas y patios de recreo durante el curso escolar, pueden correr el
riesgo de inhalar gases y partículas potencialmente nocivos, lo que podría repercutir negativamente
en su salud y su rendimiento académico. Se realizó un estudio de biomonitorización en 143 niños de
tres colegios. Dos de los colegios se consideraron expuestos a compuestos orgánicos volátiles (COV)
y estaban situados a 50 y 300 metros de gasolineras. El otro colegio, que no se consideraba expuesto,
estaba situado a 450 metros. Con la excepción de MN, los biomarcadores de daño genotóxico fueron
en general más elevados (p>0,05) en el colegio situado a 50 metros de una gasolinera que, en el grupo
de control, aunque los resultados fueron menos claros en el colegio situado a 300 metros. Para todos
los biomarcadores (KR, CC, PN y KL), el colegio situado a 50 metros de la fuente de emisiones
presentaba mayores niveles de citotoxicidad (p <0,05). Este es el primer estudio que relaciona la
exposición a hidrocarburos volátiles de la gasolina con daños genotóxicos en niños, y sugiere
fuertemente la necesidad de modificar las leyes de urbanismo para frenar el deterioro de la salud
infantil.
Palabras clave: compuestos orgánicos volátiles, micronúcleos, anomalías nucleares,
estaciones de servicio, contaminación atmosférica
Todo el contenido de LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades,
publicado en este sitio está disponibles bajo Licencia Creative Commons.
Cómo citar: García Zarate, M. A., Arellano García, M. E., González Acevedo, Z. I., & Torres Bugarín, O.
(2024). Oral epithelial cells of schoolchildren exposed to air pollution may develop cytotoxic and
genotoxic damage. LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades 5 (4), 4084
4101. https://doi.org/10.56712/latam.v5i4.2550
LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades, Asunción, Paraguay.
ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4086.
INTRODUCTION
School grounds air quality has received attention from professionals and researchers in the last few
years (USEPA, 2011). After their homes, school is the most important place for children’s development
since they spend more than 800 hours a year in them. In addition, children represent a potentially
vulnerable population and specifically susceptible to the exposure of contaminants which may affect
their health and performance as students (Neidell, 2004; Stafford, 2015; Annesi-Maesano, 2013;
Salthammer, 2016; Daisey, 2003).
The time of exposure to manifest symptoms or illness vary according to various factors such as society,
age and economy (Peled, 2011), as well as the type of contaminant such as carbon dioxide (CO2),
volatile organic compounds (VOC) and the particles (PM2.5 and PM10). These have been associated
with the development of respiratory problems and other adverse side effects in children (Madureira,
2015; Propper, 2015; Zhao, 2016).
The Health Secretariat of Mexico has been working on reducing preventable illness through vaccination
of children less than 8 years of age which protects them against 13 different illnesses. Even so,
nowadays researchers have shown that the incidence of illness in children with asthma, cancer,
leukemia, brain cancer, ADHD, diabetes and obesity (Safer Chemicals, Healthy Families de la Coalition,
2012), have been rising and this is directly linked to the exposure to chemical substances in the
environment (Pelallo-Martinez, 2014; Laborde, 2015; Di Renzo, 2015; Calderon-Garcidueñas, 2015; Liu,
2014; Currie, 2013). Therefore, eliminating this exposure to environmental chemical substances in
children is still a major objective for public health.
Environmentalists and advocates for vulnerable groups like children, older people and
immunocompromised people indicate that the development of public health policies do not take into
account children being exposed to chemical substances and federal authorities cannot see the deathly
effects the exposure to volatile organic compounds (VOC) can bring. Within the most prominent
compounds are benzene, ethylbenzene, toluene and xylene (BTEX) which individually create genotoxic,
cancerous, haematotoxic, nephrotoxic, neurotoxic effects or act as endocrine disruptors (ATSDR, 2004)
among the children in the urban area.
Children present biological characteristics that increase their vulnerability to the acute and chronic
effects of environmental toxins (Wild, 2003; Garry, 2004; Neri, 2006a) that may occur through various
means: inhalation, ingestion or dermic absorption, and it include the prenatal stage (Slate, 2011; Peters,
2014; Bailey, 2011; Garlantezec, 2009; Esplugues, 2007; Miligi, 2013). For example, childhood leukemia
is the most common type of cancer among children (Howlader et al., 2012); the most common type of
sarcoma is acute lymphoblastic leukemia (ALL) which represents 78% of the cases in children; followed
by acute myeloid leukemia (AML) which constitutes 16% of leukemia cases in children (Ries et al.,
1999).
Various authors have reported a positive association to exposure of BTEX in the mother during
pregnancy due to the vulnerability of the fetus to some toxic agents in the environment where
chromosomal translocation in the blood has been identified in new born children (Wiemels et al., 1999;
Wiemels et al., 2002; Shrestha et al., 2014; Breslow et al., 1993; Selevan et al., 2000). Benzene, a
dangerous component found in gasoline, is a genotoxic group 1 human carcinogen (Loomis, 2017;
Tunsaringkarn, 2011). Prolonged exposure to low levels of benzene in work environment and the
environment (Roma-Torres, 2006), may lead to ruptured in the DNA, micronuclei and chromosomal
abnormality (Fracasso, 2010; Angelini, 2011). Therefore, the genotoxic effects of benzene could be
associated to DNA damage (Pandey, 2008).
LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades, Asunción, Paraguay.
ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4087.
In this work, the cytotoxic and genotoxic damage has been measured through biomonitoring of the oral
mucus in groups of children and applying biomarkers through micronuclei (MN). This technique
enables the work with different types of cells such as epithelial cells (Lacerda, 2015; Acito 2022; Çelik,
2003; Carere, 1995; Benites, 2006; Hallare, 2009; Fenech M., 1993; Fenech M. et al., 1999; Fenech M.,
2000; Zalacain M. et al., 2005, Neri M. et al., 2006b; Fenech M. et al., 2007; Holland N. et al., 2008), to
determine the genotoxicity and damage to the DNA (Angelini, 2012; Bagryantseva, 2010; Rekhadevi,
2010) in the population exposed. Aside from the lack of regulation in the matter, the risk evaluation has
not been researched because there is a lack of data in the levels of benzene in the rest of the urban
population.
In this study, the relationship between air pollution and (chronic) human exposure to the contaminants
has been analyzed, focusing on the schools in which children remain from 5 to 7 hours daily (except for
weekends and holidays). The main intention is to evaluate the measure in which the exposure of people
to these contaminants seems to become affected while they remain in the area. A Geographic
Information System (GIS) has been used in order to investigate the relationship between environmental
factors and the damage incidences in micronuclei. The risk was estimated using the data on BTEX
distribution for each gas station (GS) in levels of AGEB and there was biomonitoring of 143 children of
school age in areas exposed and not exposed to GS. Lastly, there was a correlation between
determining the vulnerable areas and the genotoxic damage to define the risk. With this research, it is
expected to provide technical information to aid public policies that protect children living in the areas
potentially exposed to gas stations.
METHODOLOGY
Two procedures were performed to carry out this study. At the beginning, it was necessary to estimate
the amount of volatile organic compounds (VOC) by emissions from service stations in each school in
the urban area of Ensenada, Baja California, Mexico, using a geographic information system (GIS) with
QGIS software 3.34.5 On the other hand, to determine the biomarkers of cytotoxicity and genotoxicity
of school children, we followed the procedures of the oral micronucleus cytome assay (Fenech, 2007);
finally a nonparametric statistical analysis was applied to compare the cyto-genotoxic biomarkers of
children in school who are or are not exposed to VOC.
VOC in schools : To estimate the amount of volatile organic compounds (VOC) in each school, it was
necessary to build a database that was based on the annual sales reports of each service station for
the years 2010, 2011 and 2012, provided by the Mexican company that distributes fuels in Mexico
(Petróleos Mexicanos, PEMEX), and information on housing, population and urban equipment
contained in the units known as the Basic Geo-statistical Area (AGEB) compiled from the Statistics and
Geography National Institute (Instituto Nacional de Estadística y Geografia, INEGI) website. With these
two data sources it was possible to feed a geographic information system (GIS) with the software QGIS
3.34.5.
The emissions from gas stations were measured using the factor of emission (FE), which rises to
44.50x10-5 kg L-1 day-1, by Garcia-Zarate et al. (2015), which is the average quantity of volatile organic
compounds (VOC) that each gas station throws into the atmosphere in Baja California as a result of the
loading and unloading processes (Radian International 1996). This number was estimated based on
the chapter AP-42 published in the Environmental Protection Agency (EPA; method 18) of the United
States (US EPA, 1995, 1995ª; EPA, 1973, 2003). By other hand, the method used to determine the VOC
from area sources by the Secretariat of Labor and Social Benefits (Secretaria del Trabajo y Prevision
Social or STPS), NOM-010-STPS-1999. This estimator was important because it allowed for the risk
zones by gas station proximity to be determined according to the dispersion model resulting from the
annual sales volume and the weather conditions in the area of study.
LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades, Asunción, Paraguay.
ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4088.
The values attained from the concentrations of normalized benzene, toluene, ethylbenzene and xylene
(BTEX) came as a result of the dispersion model, and using maps, the polygons with different risk levels
to the population and schools were gathered for each station within the urban area.
Similarly, data from the school’s potentially exposed and not exposed population, healthy children of
schooling age, enrolled in the levels of elementary and middle school in Ensenada, Baja California, was
incorporated. Figure 1 shows the location of the GS and schools, as well as the Unit of Support Services
or Regular Education (Unidades de Servicios de Apoyo a la Educacion Regular USAER-SEP) that helps
schools and students in need in Ensenada, Baja California. The selection of the groups of children to
make the biomonitoring of genotoxicity and cytotoxicity is based on this model.
Figure 1
Location of schools and USAER-SEP centers within a radius of 300m from the gas stations in the urban
area of Ensenada, Baja California
Biomonitoring of cytotoxicity and genotoxicity
In the second part of this study there was a biomonitoring of genotoxic damage in 143 children of
schooling age corresponding to three groups: the first two are considered exposed and the third as a
control group. The following criteria were considered to make the selection: approval from the children
and consent from their parents to include their children in the study. There was a micronuclei (MN)
assay on oral epithelial cells (Thomas, 2009; Bonassi, 2011) frequently used in evaluations of people
exposed to organic volatile compounds and another cito-genotoxic agents (Patlolla B. et al., 2005).
Briefly, each child rinsed their mouth twice using drinking water, there were two samples taken of the
exfoliated buccal cells by gently scraping the inside of the cheek, a extend was made in slide and dry
at air, fixated in 80% ethanol and staining with eosin and fast green. 2000 epithelial cells were read in
the smears with optical microscope at 100X registering the different biomarkers of genotoxic and
cytotoxic damage: micronuclei (MN), nuclear gems or broken eggs (NL), basal cells (BC), binucleated
cells (BN), condensate chromatin (CC), karyorrhexis (KR), karyolysis (KL) and Pyknosis (PN) (Torres-
LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades, Asunción, Paraguay.
ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4089.
Bugarin, 2013, 2007; Holland et al., 2008; Heddle et al., 1991; Violante, 2012; Grover, 2012; Lacerda,
2015; Ceretti,, 2014; Feretti, 2014; Martins et al. 2009; Majer, 2001).
The amount of nuclear abnormalities was coded into an Excel© sheet. To guarantee homogeneity in
the variances and making the comparisons by confidence intervals viable, there was an arcsine
transformation of concepts and methodologies given by Bartlett (1936), Anscombe (1948) and
Zar (1984) for the variables distributed according to the Poisson distribution, based on the following
expression:
󰇛
󰇜 





The transformed data was analyzed using the Graph-Pad-Prism© v7 program and a Kruskal-Wallis test
with Bonferroni post hoc multiple comparison test was performed to compare the groups of children
being studied.
RESULTS
The children at the "Justo Sierra" school (Escuela Primaria Urbana Estatal “Justo Sierra”), located 50 m
from a gas station, formed the first group with 48 children exposed (n = 48), 18 children and 30 girls
with an average age of 10.17 ± 0.66. Group two was "Sec. 9" (Escuela Secundaria Urbana Estatal
Numero 9) at 300 m from the service station with 55 children exposed, 31 boys and 24 girls with an
average age of 13.96 ± 0.43. A third group consisting of 40 children was the control group (not exposed)
located 425 meters from the nearest service station with 23 children and 17 girls, with an average age
of 10.50 ± 0.43.
Following the suggestions of different authors (Kales, 1997; Horton, 2003; Terres, 2010; Silva 2009;
Santos, 2013; Karakitsios, 2007; Correa, 2012; Hystad, 2011; Beltrán, 1996; Zagal, 1996; CENAPRED,
2001; Arcos, 2007; Rivera, 2006), the type of pollutant, the type of exposure (point source or diffuse)
and the location of schools within a 300 m radius of each petrol station were used to determine the
level of exposure in the geographical scenarios of this study. It was found that many petrol stations in
cities are located close to residential buildings or educational institutions. The locations of the schools
with the highest emissions from petrol stations in relation to the emission factor are shown in Figure
2.
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ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4090.
Figure 2
Location of schools in sampling
The increase in nuclear abnormalities could be due to regular exposure to gasoline vapours (BTEX)
from the GS, which contain genotoxic compounds and alter the structural make-up of all cells in the
bone marrow (Bukvic, 1998). They are also leukaemogenic and anaplastic, which has shown that there
is a significant difference in the rate of micronuclei and nuclear abnormalities between the population
exposed to BTEX in the environment from GS (Table I) and the unexposed group. In Justo Sierra, the
percentage of students of both sexes exposed to the contaminant (F/M) was 30/18 (65%/27%), while
in the unexposed group it was 17/23 (43%/57%).
Table 1
The mean frequency of micronuclei per 2000 cells of the buccal mucosa in the groups studied
MN / 2000
Group
Men
Women
n
Distance to GS
(m)
min
max
cases
Justo sierra
18
30
48
50
0
7
20
Sec. No. 9
31
24
55
300
0
3
23
UNEXPOSED
POPULATION
23
17
40
425
0
1
3
Exposure-induced damage to genetic material may lead to genotoxic or cytotoxic events in epithelial
cells where the primary chromosomal abnormalities required for classification have been observed.
According to the exposure to genotoxic and cytotoxic damage leading to cell death, such as necrosis
and apoptosis, Table II shows the mean and standard error for each cellular abnormality. (Filipo, 2018;
Ceretti, 2014).
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ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4091.
Table 2
Basic statistics for transformed variables by each one nuclear anomalies for three of children groups
Type of
damage
Biomarker
School
Mean
Standard
error
Inferior
Confidential
Limit (95%)
Superior
Confidential
Limit (95%)
N
Genotox
icity
Micronuclei
(MN)
Justo Sierra
1
0.22
0.57
1.43
48
Sec. 9
0.89
0.2
0.49
1.29
55
Control
0.65
0.24
0.19
1.12
40
Lobulated
Nucleus
(LN)
Justo Sierra
1.33
0.22
0.9
1.76
48
Sec. 9
Control
1.37
0.61
0.2
0.24
0.97
0.14
1.77
1.08
55
40
Effects
in
cellular
cycles
Binucleated
(BN)
Justo Sierra
2.74
0.22
2.31
3.17
48
Sec. 9
2.19
0.2
1.79
2.58
55
Control
1.3
0.24
0.83
1.77
40
Cytotoxi
city:
Necrosi
s and
Apoptos
is
Karyorrhexis
(KR)
Justo Sierra
Sec. 9
2.75
1.35
0.22
0.2
2.32
0.95
3.17
1.74
48
55
Control
1.16
0.24
0.69
1.63
40
Justo Sierra
6.52
0.22
6.09
6.95
48
Condensed
Chromatin
(CC)
Sec. 9
Control
3.95
0.68
0.2
0.24
3.55
0.22
4.35
1.15
55
40
Pyknosis
(PN)
Justo Sierra
3.17
0.22
2.74
3.6
48
Sec. 9
Control
2.33
1.14
0.2
0.24
1.93
0.67
2.73
55
1.61
40
Karyolysis
(KL)
Justo Sierra
2.93
0.22
2.51
3.36
48
Sec. 9
2.6
0.2
2.2
3
55
Control
2
0.24
1.54
2.47
40
The frequency of micronuclei and nuclear abnormalities in the control group is shown in graphic 1, and
the exposed groups - including the Justo Sierra and Sec. No. 9 boys - show that those exposed to BTEX
have significantly more DNA damage than the control group.
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ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4092.
Graphic 1
Biomarkers of genotoxic and cytotoxic damage in 2000 cells in children of the "Justo Sierra" and "Sec.
No. 9" groups and control
The vertical lines express the standard error P ± 0.95. The asterisks and "ns" indicate significance level
with the Bonferroni multiple comparisons test against the control group.
Analysis of exfoliated cells from buccal mucus reveals evidence of other nuclear changes, including
binucleated cells, karyorrhexis and karyolysis. According to Carlin et al (2010), the presence of
binucleated cells is thought to be a sign of cytotoxicity, DNA damage and cell death. In addition,
chromosomal abnormalities caused by DNA breakage are also thought to be caused by karyorrhexis
and karyolysis, which can result in both minor and major structural changes or be removed by the
mechanism of cellular repair through cell death, which is planned as an indicator of apoptosis (Tolbert,
1992). Only that children are more susceptible than adults has been suggested by previous research
(Lakhanisky, 1993; Laurent, 1993; Klemans, 1995).
Apoptotic cells differ from necrotic cells in that the latter undergo "passive" cell death, including a
rupture of the plasma membrane that releases intracellular material and triggers an inflammatory
response (Wyllie, 1980). On the other hand, apoptosis, also known as physiological death, is an active
process involving protein synthesis and characterised by cytoplasmic and nuclear condensation
(pyknosis). The final stage of internucleosomal fragmentation and DNA rupture occurs in the
cytoplasm, where there is nuclear chromatin condensation, nuclear disintegration, reduced damage,
cytoplasmic and organelle compaction, and a bubble-like membrane (Wyllie, 1984). On the other hand,
an increase in apoptosis could be a sign of genotoxic damage (Tolbert, 1992). It has been said that
apoptosis occurs by ionizing radiation, as well as, chemical compounds that attach to the DNA or by
genetic deregulation. It can also act as a recognition mechanism eliminating the cells with genetic
damage. In this way, the excess of apoptosis could indicate genotoxic damage (Tolbert, 1992).
Aneuploidies (both germinal and somatic) are associated with significant genetic changes linked to
spontaneous miscarriage, mental retardation and cancer, although rupture can lead to cell death
(Hagmar, 1994).
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ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4093.
CONCLUSIONS
The unplanned growth of urban areas has led to the inappropriate use of land for various economic
activities, which becomes problematic over time. The use of GIS can help predict the impact on
educational centres. Based on the distance from the GS, the vulnerability of schools is strongly related
to their location.
This is the first study carried out on a group of children using the MN test, from which we can say that
the genotoxic effect is caused by exposure to petrol emissions (BTEX). The test for micronuclei in
buccal epithelial cells is one of the most sensitive methods used to measure the rate of DNA damage
in the human population, as it is relatively easy to determine damage in micronuclei compared to other
methods, such as chromosomal aberrations. It can be used not only to identify groups at risk of
developing cancer, but also to identify individuals who are susceptible to developing cancer.
The results indicate that people exposed to the chemicals of the GS are groups at risk, taking into
account that they are strong mutagens and that the emission of these products has genotoxic and
cytotoxic properties, as demonstrated by Hadnagy (1988, 1989) in buccal cells. It was found that the
frequency of micronuclei and nuclear abnormalities, genotoxic damage and health consequences
increased with exposure, in correlation with the increasing number of petrol stations in urban areas.
The levels of apoptosis observed in this study are significantly higher in the exposed group, as observed
by Revazova et al. (2001). All the cytotoxic and mutagenic changes observed in this document are
related to the strength of petrol and its components, especially benzene.
The methodology used in the GIS is not difficult to apply and the results can be considered for
prevention, territorial planning and minimisation of risks due to the presence of GS within a radius of
300 m around schools.
These factors could contribute to a chronic exposure at low concentrations, posing a threat to the
health, productivity and efficiency of children in neighbouring schools, considered a public health issue
and detectable with genotoxicity tests.
The public health sector can play a major role in promoting the prevention of exposure to air pollution.
Improving air quality should be considered as an important part of public policy making in various
economic sectors. The effects on health are highly unequal: air pollution combines with other aspects
to create a disproportionate morbidity burden for low-income groups. All this should be taken into
account when designing and implementing long-term policies and programmes to reduce air pollution
and improve overall health. The results suggest the need for environmental policies to reduce the
burden of GHS, which results from neglecting the vulnerability of children when setting limits for
exposure to pollutants in urban areas. It is known that among the most serious diseases are genetic
diseases caused by genotoxic effects on somatic cells, such as cancer. It is therefore very important
to publicise these studies in order to encourage the public authorities to inform themselves of the
possible health risks when authorising filling stations and to find solutions that could help to maintain
the environmental balance in urban areas.
LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades, Asunción, Paraguay.
ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4094.
REFERENCES
Angelini, S., Kumar, R., Bermejo, J. L., Maffei, F., Barbieri, A., Graziosi, F., & Hrelia, P. (2011). Exposure to
low environmental levels of benzene: evaluation of micronucleus frequencies and S-phenylmercapturic
acid excretion in relation to polymorphisms in genes encoding metabolic enzymes. Mutation
Research/Genetic Toxicology and Environmental Mutagenesis, 719(1), 7-13.
Angelini, S., Maffei, F., Bermejo, J. L., Ravegnini, G., L’Insalata, D., Cantelli-Forti, G., & Hrelia, P. (2012).
Environmental exposure to benzene, micronucleus formation and polymorphisms in DNA-repair genes:
a pilot study. Mutation Research/Genetic Toxicology and Environmental Mutagenesis, 743(1), 99-104.
Annesi-Maesano, I., Baiz, N., Banerjee, S., Rudnai, P., Rive, S., & SINPHONIE Group. (2013). Indoor air
quality and sources in schools and related health effects. Journal of Toxicology and Environmental
Health, Part B, 16(8), 491-550.
Anscombe, F. J. (1948). The transformation of Poisson, binomial and negative-binomial
data. Biometrika, 35(3/4), 246-254.
Arcos, M., Treviño, C., Espinosa, B., Balboa, R. y Medina, E. (2007). Riesgos químicos, 1ª edición, Centro
Nacional de Prevención de Desastres, Secretaría de Gobernación, D. F., México.
ATSDR (2004). Agency for Toxic Substances and Disease Registry. Interaction Profile for Benzene,
Toluene, Ethylbenzene, and Xylenes (BTEX). Atlanta: U.S. Department of Health and Human Services;
2004 May. Retrieved from http://www.atsdr.cdc.gov/interactionprofiles/IP-btex/ip05.pdf.
Bagryantseva, Y., Novotna, B., Rossner Jr, P., Chvatalova, I., Milcova, A., Svecova, V., & Sram, R. J. (2010).
Oxidative damage to biological macromolecules in Prague bus drivers and garagemen: impact of air
pollution and genetic polymorphisms. Toxicology letters, 199(1), 60-68.
Bailey, H. D., de Klerk, N. H., Fritschi, L., Attia, J., Daubenton, J. D., Armstrong, B. K., & Milne, E. (2011).
Refuelling of vehicles, the use of wood burners and the risk of acute lymphoblastic leukaemia in
childhood. Paediatric and perinatal epidemiology, 25(6), 528-539.
Benites, C. I., Amado, L. L., Vianna, R. A. P., & da Graça Martino-Roth, M. (2006). Micronucleus test on
gas station attendants. Genetics and Molecular Research, 5(1), 45-54.
Bartlett, M. (1936). The square root transformation in analysis of variance. Supplement to the Journal
of the Royal Statistical Society, 3(1), 68-78.
Bonassi, S., Coskun, E., Ceppi, M., Lando, C., Bolognesi, C., Burgaz, S., ... & Carnesoltas, D. (2011). The
HUman MicroNucleus project on eXfoLiated buccal cells (HUMNXL): The role of life-style, host factors,
occupational exposures, health status, and assay protocol. Mutation Research/Reviews in Mutation
Research, 728(3), 88-97.
Breslow, N., Olshan, A., Beckwith, J. B., & Green, D. M. (1993). Epidemiology of Wilms tumor. Medical
and pediatric oncology, 21(3), 172-181.
Beltran, L. (1996). Evaluación de la peligrosidad en un parque industrial (Caso de estudio: Ciudad
Industrial del Valle de Cuernavaca, Mor.). Tesis de Maestría en Ingeniería Ambiental. División de
Estudios de Posgrado de la Facultad de Ingeniería, UNAM. México.
Bukvic, N., Bavaro, P., Elia, G., Cassano, F., Fanelli, M., & Guanti, G. (1998). Sister chromatid exchange
(SCE) and micronucleus (MN) frequencies in lymphocytes of gasoline station attendants. Mutation
Research/Genetic Toxicology and Environmental Mutagenesis, 415(1), 25-33.
LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades, Asunción, Paraguay.
ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4095.
Calderón-Garcidueñas, L., Kulesza, R. J., Doty, R. L., D'Angiulli, A., & Torres-Jardón, R. (2015). Megacities
air pollution problems: Mexico City Metropolitan Area critical issues on the central nervous system
pediatric impact. Environmental research, 137, 157-169.
Carlin, V., Artioli, A. J., Matsumoto, M. A., Borgo, E., Oshima, C. T. F., & Ribeiro, D. A. (2010).
Biomonitoring of DNA damage and cytotoxicity in individuals exposed to cone beam computed
tomography. Dentomaxillofacial Radiology. 39: 295-299.
Carere, A., Antoccia, A., Crebelli, R., Degrassi, F., Fiore, M., Iavarone, I., ... & Zijno, A. (1995). Genetic
effects of petroleum fuels: cytogenetic monitoring of gasoline station attendants. Mutation
Research/Fundamental and Molecular Mechanisms of Mutagenesis, 332(1), 17-26.
Ceretti, E., Feretti, D., Viola, G. C. V., Zerbini, I., Limina, R. M., Zani, C., ... & Gelatti, U. (2014). DNA damage
in buccal mucosa cells of pre-school children exposed to high levels of urban air pollutants. PLoS
One, 9(5), e96524.
Centro Nacional de Prevención de Desastres CENAPRED (2001). Diagnóstico de Peligros e
Identificación de Riesgos de Desastres en México: Atlas Nacional de Riesgos de la República Mexicana,
1ª edición, Centro Nacional de Prevención de Desastres, Secretaría de Gobernación, D. F., México.
Çelik, A., Çavaş, T., & Ergene‐Gözükara, S. (2003). Cytogenetic biomonitoring in petrol station
attendants: micronucleus test in exfoliated buccal cells. Mutagenesis, 18(5), 417-421.
Loomis, D., Guyton, K. Z., Grosse, Y., El Ghissassi, F., Bouvard, V., Benbrahim-Tallaa, L., ... & Straif, K.
(2017). Carcinogenicity of benzene. The Lancet Oncology, 18(12), 1574-1575.
Correa SM, Arbilla G, Marques MRC, Oliveira KMPG, (2012). The impact of BTEX emissions from gas
stations into the atmosphere. Atmospheric Pollution Research; 3: 163-9.
Currie, J. (2013). Pollution and Infant Health. Child development perspectives, 7(4), 237-242.
Daisey, J. M., Angell, W. J., & Apte, M. G. (2003). Indoor air quality, ventilation and health symptoms in
schools: an analysis of existing information. Indoor air, 13(1), 53-64.
Acito, M., Fatigoni, C., Villarini, M., & Moretti, M. (2022). Cytogenetic effects in children exposed to air
pollutants: A systematic review and meta-analysis. International Journal of Environmental Research
and Public Health, 19(11), 6736.
Di Renzo, G. C., Conry, J. A., Blake, J., DeFrancesco, M. S., DeNicola, N., Martin, J. N.,... & Woodruff, T. J.
(2015). International Federation of Gynecology and Obstetrics opinion on reproductive health impacts
of exposure to toxic environmental chemicals. International Journal of Gynecology & Obstetrics, 131(3),
219-225.
Environmental Protection Agency, EPA United States Environmental Protection Agency, (1973).Guide
for compiling a comprehensive emission inventory. Washington, D.C;
Environmental Protection Agency, EPA, (2003). Air Quality Index. A guide to Air quality and your health.
Washington: EPA, (EPA-454/k-03-002)
Esplugues, A., Fernández-Patier, R., Aguilera, I., Iñíguez, C., García Dos Santos, S., Aguirre Alfaro, A., &
Ballester, F. (2007). Exposición a contaminantes atmosféricos durante el embarazo y desarrollo
prenatal y neonatal: protocolo de investigación en el proyecto INMA (Infancia y Medio Ambiente).
Gaceta Sanitaria, 21(2), 162-171.
LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades, Asunción, Paraguay.
ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4096.
Fenech, M. (1993). The cytokinesis-block micronucleus technique: a detailed description of the method
and its application to genotoxicity studies in human populations. Mutation Research/Fundamental and
Molecular Mechanisms of Mutagenesis, 285(1), 35-44.
Fenech, M. (2007). Cytokinesis-block micronucleus cytome assay. Nature protocols, 2(5), 1084-1104.
Fenech, M., Holland, N., Chang, W. P., Zeiger, E., & Bonassi, S. (1999). The HUman MicroNucleus
Projectan international collaborative study on the use of the micronucleus technique for measuring
DNA damage in humans. Mutation Research/Fundamental and Molecular Mechanisms of
Mutagenesis, 428(1), 271-283.
Fenech, M. (2000). The in vitro micronucleus technique. Mutation Research/Fundamental and
Molecular Mechanisms of Mutagenesis, 455(1), 81-95.
Feretti, D., Ceretti, E., De Donno, A., Moretti, M., Carducci, A., Bonetta, S., ... & MAPEC_LIFE Study Group.
(2014). Monitoring air pollution effects on children for supporting public health policy: the protocol of
the prospective cohort MAPEC study. BMJ open, 4(9), e006096.
Filho, A. P., Silveira, M. A., do Nascimento, C. B., & d’Arce, L. P. (2018). Integrative study of cell damage
and cancer risk in gas station attendants. International journal of environmental health research, 28(1),
1-7.
Fracasso, M. E., Doria, D., Bartolucci, G. B., Carrieri, M., Lovreglio, P., Ballini, A., ... & Manno, M. (2010).
Low air levels of benzene: correlation between biomarkers of exposure and genotoxic effects.
Toxicology letters, 192(1), 22-28.
García-Zarate MA, Arellano García ME, Daessle Heuser LW, Villada Canela M, Quintero Núñez (2015).
Mapa cualitativo para el análisis de riesgo por BTEX por proximidad con gasolineras en la ciudad de
Ensenada, Baja California, México. Revista de Salud Ambiental, 15(1), 4-12.
Garlantézec, R., Monfort, C., Rouget, F., & Cordier, S. (2009). Maternal occupational exposure to solvents
and congenital malformations: a prospective study in the general population. Occupational and
environmental medicine, 66(7), 456-463.
Garry, V. F. (2004). Pesticides and children. Toxicology and applied pharmacology, 198(2), 152-163.
Grover, S., Mujib, A., Jahagirdar, A., Telagi, N., & Kulkarni, P. G. (2012). A comparative study for selectivity
of micronuclei in oral exfoliated epithelial cells. Journal of Cytology, 29(4), 230.
Hadnagy, W., & Seemayer, N. H. (1988). Cytotoxic and genotoxic effects of extract of particulate
emission from a gasoline‐powered engine. Environmental Mutagenesis, 12(4), 385-396.
Hadnagy, W., & Seemayer, N. H. (1989). Genotoxicity of particulate emissions from gasoline-powered
engines evaluated by short-term bioassays. Experimental pathology, 37(1), 43-50.
Hagmar, L., Brøgger, A., Hansteen, I. L., Heim, S., Högstedt, B., Knudsen, L., ... & Reuterwall, C. (1994).
Cancer risk in humans predicted by increased levels of chromosomal aberrations in lymphocytes:
Nordic study group on the health risk of chromosome damage. Cancer research, 54(11), 2919-2922.
Hallare, A. V., Gervasio, M. K. R., Gervasio, P. L. G., & Acacio-Claro, P. J. B. (2009). Monitoring
genotoxicity among gasoline station attendants and traffic enforcers in the City of Manila using the
micronucleus assay with exfoliated epithelial cells. Environmental monitoring and assessment, 156(1-
4), 331-341.
LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades, Asunción, Paraguay.
ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4097.
Heddle, J. A., Cimino, M. C., Hayashi, M., Romagna, F., Shelby, M. D., Tucker, J. D., ... & MacGregor, J. T.
(1991). Micronuclei as an index of cytogenetic damage: past, present, and future. Environmental and
molecular mutagenesis, 18(4), 277-291.
Holland, N., Bolognesi, C., Kirsch-Volders, M., Bonassi, S., Zeiger, E., Knasmueller, S., & Fenech, M.
(2008). The micronucleus assay in human buccal cells as a tool for biomonitoring DNA damage: the
HUMN project perspective on current status and knowledge gaps. Mutation Research/Reviews in
Mutation Research, 659(1-2), 93-108.
Horton, D. K., Berkowitz, Z., Haugh, G. S., Orr, M. F. y Kaye, W. E. (2003). “Acute public health
consequences associated with hazardous substances released during transit, 1993-2000”, Journal of
Hazardous Materials, Vol. 98, No.1-3, pp. 161-175.
Howlader, N., Noone, A. M., Krapcho, M., Neyman, N., Aminou, R., Altekruse, S. F., & Mariotto, A. (2012).
SEER cancer statistics review, 19752009 (vintage 2009 populations). Bethesda, MD: National Cancer
Institute; 2012. Lung cancer.
Hystad, P., Setton, E., Cervantes, A., Poplawski, K., Deschenes, S., Brauer, M., Demers, P. 2011). Creating
national air pollution models for population exposure assessment in Canada. Environmental health
perspectives, 119(8), 1123.nei
Kales, S. N., Polyhronopoulos, G. N., Castro, M. J., Goldman, R. H. y Christiani, D. C. (1997). “Injuries
caused by hazardous materials accidents”, Annals of Emergency Medicine, Vol. 30, No. 5, pp. 598-603.
Karakitsios, S.P., Delis, V.K., Kassomenos, P.A., Pilidis, G.A., (2007). Contribution to ambient benzene
concentrations in the vicinity of petrol stations: estimation of the associated health risk. Atmospheric
Environment; 41, 1889 -1902
Klemans, W., Vleminckx, C., Schriewer, L., Joris, I., Lijsen, N., Maes, A.,... & Ros, Y. (1995). Cytogenetic
biomonitoring of a population of children allegedly exposed to environmental pollutants Phase 2:
Results of a three-year longitudinal study. Mutation Research/Genetic Toxicology, 342(3), 147-156.
Lacerda, L. P., Dantas, E. B., dos Santos Cerqueira, G., Peron, A. P., & Castro, J. M. (2015). Occupational
toxicology study emphasizing the cytotoxic and mutagenic activity among workers exposed to
gasoline. Biotemas, 28(3), 135-141.
Laborde, A., Tomasina, F., Bianchi, F., Bruné, M. N., Buka, I., Comba, P., ... & Iavarone, I. (2015). Children's
health in Latin America: the influence of environmental exposures. Environmental Health Perspectives
(Online), 123(3), 201.
Lakhanisky, T., Bazzoni, D., Jadot, P., Joris, I., Laurent, C., Ottogali, M., ... & Vleminckx, C. (1993).
Cytogenetic monitoring of a village population potentially exposed to a low level of environmental
pollutants. Phase 1: SCE analysis. Mutation Research/Genetic Toxicology, 319(4), 317-323.
Laurent, C., Lakhanisky, T., Jadot, P., Joris, I., Ottogali, M., Planard, C., ... & Ros, Y. (1993). Increased
sister chromatid exchange frequencies observed in a cohort of inhabitants of a village located at the
boundary of an industrial dumping ground: phase I. Cancer Epidemiology Biomarkers & Prevention, 2(4),
355-362.
Liu, J., & Lewis, G. (2014). Environmental toxicity and poor cognitive outcomes in children and adults.
Journal of environmental health, 76(6), 130.
LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades, Asunción, Paraguay.
ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4098.
Madureira, J., Paciência, I., Rufo, J., Ramos, E., Barros, H., Teixeira, J. P., & de Oliveira Fernandes, E.
(2015). Indoor air quality in schools and its relationship with children's respiratory
symptoms. Atmospheric Environment, 118, 145-156.
Majer, B. J., Laky, B., Knasmüller, S., & Kassie, F. (2001). Use of the micronucleus assay with exfoliated
epithelial cells as a biomarker for monitoring individuals at elevated risk of genetic damage and in
chemoprevention trials. Mutation Research/Reviews in Mutation Research, 489(2), 147-172.
Martins RA, Gomes GA, Aguiar O Jr, Ribeiro DA (2009) Biomonitoring of oral epithelial cells in petrol
station attendants: comparison between buccal mucosa and lateral border of the tongue. Environ Int
35:10621065
Miligi, L., Benvenuti, A., Mattioli, S., Salvan, A., Tozzi, G. A., Ranucci, A.,... & SETIL Working Group. (2013).
Risk of childhood leukaemia and non-Hodgkin's lymphoma after parental occupational exposure to
solvents and other agents: the SETIL Study. Occupational and environmental medicine, oemed-2012.
Neidell, M. J. (2004). Air pollution, health, and socio-economic status: the effect of outdoor air quality
on childhood asthma. Journal of health economics, 23(6), 1209-1236.
Neri, M., Bonassi, S., Knudsen, L. E., Sram, R. J., Holland, N., Ugolini, D., & Merlo, D. F. (2006a). Children's
exposure to environmental pollutants and biomarkers of genetic damage: I. Overview and critical
issues. Mutation Research/Reviews in Mutation Research, 612(1), 1-13.
Neri, M., Ugolini, D., Bonassi, S., Fucic, A., Holland, N., Knudsen, L. E., & Merlo, D. F. (2006b). Children's
exposure to environmental pollutants and biomarkers of genetic damage: II. Results of a
comprehensive literature search and meta-analysis. Mutation Research/Reviews in Mutation
Research, 612(1), 14-39.
NOM-010-STPS-1999 Secretaría de Trabajo y Previsión Social. Norma Oficial Mexicana, condiciones de
seguridad e higiene en los centros de trabajo donde se manejen, transporten, procesen o almacenen
sustancias químicas capaces de generar contaminación en el medio ambiente laboral. Diario Oficial de
la Federación 13 de marzo de 2000.
Pandey, A. K., Bajpayee, M., Parmar, D., Kumar, R., Rastogi, S. K., Mathur, N. ... & Dhawan, A. (2008).
Environmental and molecular mutagenesis, 49(9), 695-707.
Pelallo-Martínez, N. A., Batres-Esquivel, L., Carrizales-Yáñez, L., & Díaz-Barriga, F. M. (2014). Genotoxic
and hematological effects in children exposed to a chemical mixture in a petrochemical area in Mexico.
Archives of environmental contamination and toxicology, 67(1), 1-8.
Peled, R. (2011). Air pollution exposure: Who is at high risk?. Atmospheric Environment, 45(10), 1781-
1785.
Peters, S., Glass, D. C., Greenop, K. R., Armstrong, B. K., Kirby, M., Milne, E., & Fritschi, L. (2014).
Childhood brain tumours: associations with parental occupational exposure to solvents. British journal
of cancer.
Patlolla, B. P., Patlolla, A. K., & Tchounwou, P. B. (2005). Cytogenetic effects of 1, 1-dichloroethane in
mice bone marrow cells. International journal of environmental research and public health, 2(1), 101-
106.
Propper, R., Wong, P., Bui, S., Austin, J., Vance, W., Alvarado, A. ... & Luo, D. (2015). Ambient and emission
trends of toxic air contaminants in California. Environmental science & technology, 49(19), 11329-
11339.
LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades, Asunción, Paraguay.
ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4099.
Radian International (1996). "Manuales del programa de inventarios de emisiones de México: Vol. 3 -
Técnicas básicas de estimación de emisiones" . Sacramento, CA.
Rekhadevi, P. V., Rahman, M. F., Mahboob, M., & Grover, P. (2010). Genotoxicity in filling station
attendants exposed to petroleum hydrocarbons. Annals of Occupational Hygiene, 54(8), 944-954.
Revazova, J., Yurchenko, V., Katosova, L., Platonova, V., Sycheva, L., Khripach, L.... & Zhurkov, V. (2001).
Cytogenetic investigation of women exposed to different levels of dioxins in Chapaevsk town.
Chemosphere, 43(4), 999-1004.
Ries, L. A. G., Smith, M. A., Gurney, J. G., Linet, M., Tamra, T., Young, J. L., & Bunin, G. (1999). Cancer
incidence and survival among children and adolescents: United States SEER Program 1975-
1995. Cancer incidence and survival among children and adolescents: United States SEER Program
1975-1995.
Rivera, R., Arcos, M., Izcapa, C., Bravo, E., Bernabé, L., Muñoz, E., Torres, L., Zepeda, O., Andrade, E. y
López, L. (2006). Guía Básica para la Elaboración de Atlas Estatales y Municipales de Peligros y
Riesgos: Fenómenos Químicos, 1ª edición, Centro Nacional de Prevención de Desastres, Secretaría de
Gobernación, D.F., México.
Roma-Torres, J., Teixeira, J. P., Silva, S., Laffon, B., Cunha, L. M., Méndez, J., & Mayan, O. (2006).
Evaluation of genotoxicity in a group of workers from a petroleum refinery aromatics plant. Mutation
Research/Genetic Toxicology and Environmental Mutagenesis, 604(1), 19-27.
Safer Chemicals, Healthy Families Coalition. (2012). Chemicals and our health: Why recent science is
a call to action. Retrieved from http://saferchemicals.org/PDF/chemicals-and-our-health-july-2012.pdf
Salthammer, T., Uhde, E., Schripp, T., Schieweck, A., Morawska, L., Mazaheri, M., ... & Viana, M. (2016).
Children's well-being at schools: impact of climatic conditions and air pollution. Environment
international, 94, 196-210.
Santos, M. D. A., Tavora, B. E., Koide, S., & Caldas, E. D. (2013). Human risk assessment of benzene
after a gasoline station fuel leak. Revista de Saúde Pública, 47(2), 335-344.
cSelevan, S. G., Kimmel, C. A., & Mendola, P. (2000). Identifying critical windows of exposure for
children's health. Environmental health perspectives, 108(Suppl 3), 451.
Shrestha, A., Ritz, B., Wilhelm, M., Qiu, J., Cockburn, M., & Heck, J. E. (2015). Prenatal exposure to air
toxics and risk of Wilms’ tumor in 0-5 year old children. Journal of occupational and environmental
medicine/American College of Occupational and Environmental Medicine, 56(6), 573.
Silva, F.L.D., dos Santos, J.R., Moita, J.M., da Silva, R.L.G.D., Flumignan, D.L., de Oliveira, J.E. 2009.
Determination of benzene, toluene, ethylbenzene and xylenes in commercial gasoline from Piaui State.
Quimica Nova 32, 56-U64
Slate, M. E., Linabery, A. M., Spector, L. G., Johnson, K. J., Hilden, J. M., Heerema, N. A. & Ross, J. A.
(2011). Maternal exposure to household chemicals and risk of infant leukemia: a report from the
Children’s Oncology Group. Cancer Causes & Control, 22(8), 1197-1204.
Stafford, T. M. (2015). Indoor air quality and academic performance. Journal of Environmental
Economics and Management, 70, 34-50.
Terres, I.M.M., Minarro, M.D., Ferradas, E.G., Caracena, A.B., Rico, J.B. 2010. Assessing the impact of
petrol stations on their immediate surroundings. Journal of Environmental management 91, 2754-2762
LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades, Asunción, Paraguay.
ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4100.
Thomas, P., Holland, N., Bolognesi, C., Kirsch-Volders, M., Bonassi, S., Zeiger, E., ... & Fenech, M. (2009).
Buccal micronucleus cytome assay. Nature protocols, 4(6), 825.
Tolbert, P. E., Shy, C. M., & Allen, J. W. (1992). Micronuclei and other nuclear anomalies in buccal
smears: methods development. Mutation Research/Environmental Mutagenesis and Related
Subjects, 271(1), 69-77.
Torres-Bugarín, O., Covarrubias-Bugarín, R., Zamora-perez, A. L., Torres-Mendoza, B., García-Ulloa, M., &
Martínez-Sandoval, F. (2007). Anabolic-Androgenic Steroids Induce Micronuclei in Buccal Mucosa Cells
of Body Builders. British journal of sports medicine.
Torres-Bugarín, O., & Ramos-Ibarra, M. L. (2013). Utilidad de la prueba de micronúcleos y anormalidades
nucleares en células exfoliadas de mucosa oral en la evaluación de daño genotóxico y citotóxico.
International Journal of Morphology, 31(2), 650-657.
Tunsaringkarn, T., Suwansaksri, J., Soogarun, S., Siriwong, W., Rungsiyothin, A., Zapuang, K., & Robson,
M. (2011). Genotoxic monitoring and benzene exposure assessment of gasoline station workers in
metropolitan Bangkok: sister chromatid exchange (SCE) and urinary trans, trans-muconic acid (t, t-
MA). Asian Pac J Cancer Prev, 12(1), 223-7.
US EPA (United States Environmental Protection Agency), (1995). Compilation of Air Pollutant Emission
Factors AP42. 5th Edition, Office of Air Quality Planning and Standards, Research Triangle Park, NC.
US EPA (The United States Environmental Protection Agency), (1995a). Compilation of Air Pollutant
Emission FactorsStationary Point and Area Sources. Research Triangle Park, NC, AP42.
US Environmental Protection Agency (USEPA). (2011). Background Indoor Air Concentrations of
Volatile Organic Compounds in North American Residences (19902005): A Compilation of Statistics
for Assessing Vapor Intrusion. Washington, DC: Office of Solid Waste and Emergency Response.
Violante, E. Z., García, E. A., Ojinaga, L. C., Heusser, W. D., Von-Glascoe, C., Aguilera, J. C. L., & Ruiz, B.
R. (2012). Daño genético y exposición a plaguicidas en trabajadores agrícolas del Valle de San Quintín,
Baja California, México. Revista de Salud Ambiental, 12(2), 93-101.
Wiemels, J. L., Cazzaniga, G., Daniotti, M., Eden, O. B., Addison, G. M., Masera, G., ... & Greaves, M. F.
(1999). Prenatal origin of acute lymphoblastic leukaemia in children. The Lancet, 354(9189), 1499-
1503.
Wiemels, J. L., Xiao, Z., Buffler, P. A., Maia, A. T., Ma, X., Dicks, B. M. ... & Pritchard-Jones, K. (2002). In
utero origin of t (8; 21) AML1-ETO translocations in childhood acute myeloid leukemia. Blood, 99(10),
3801-3805.
Wild, C. P., & Kleinjans, J. (2003). Children and increased susceptibility to environmental carcinogens
evidence or empathy?. Cancer Epidemiology Biomarkers & Prevention, 12(12), 1389-1394.
Wyllie, A. H., Kerr, J. R., & Currie, A. R. (1980). Cell death: the significance of apoptosis. International
review of cytology, 68, 251-306.
Wyllie, A. H., Morris, R. G., Smith, A. L., & Dunlop, D. (1984). Chromatin cleavage in apoptosis: association
with condensed chromatin morphology and dependence on macromolecular synthesis. The Journal of
pathology, 142(1), 67-77.
Zagal, J. (1996). Método de evaluación de riesgos en accidentes químicos. Memorias del Simposio
regional sobre preparativos para emergencias y desastres químicos: Un reto para el siglo XXI. OPS /
LATAM Revista Latinoamericana de Ciencias Sociales y Humanidades, Asunción, Paraguay.
ISSN en línea: 2789-3855, agosto, 2024, Volumen V, Número 4 p 4101.
OMS. División de Salud y Ambiente. Programa de preparativos para situaciones de emergencia y
coordinación de socorro en casos de desastre. México, D.F., Diciembre.
Zalacain, M., Sierrasesumaga, L., & Patiño, A. (2005). El ensayo de micronúcleos como medida de
inestabilidad genética inducida por agentes genotóxicos. In Anales del sistema sanitario de
Navarra (Vol. 28, No. 2, pp. 227-236). Gobierno de Navarra. Departamento de Salud.
Zar, J.H., 1984. Biostatistical Analysis. Second Edition. Prentice-Hall Inc., Nueva Jersey, 718 pp.
Zhao, P., Cheng, Y. H., Lin, C. C., & Cheng, Y. L. (2016). Effect of resin content and substrate on the
emission of BTEX and carbonyls from low-VOC water-based wall paint. Environmental Science and
Pollution Research, 23(4), 3799-3808.
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