Residential proximity to petrol stations and risk of childhood leukemia

Malavolti, Marcella; Malagoli, Carlotta; Filippini, Tommaso; Wise, Lauren A.; Bellelli, Alessio; Palazzi, Giovanni; Cellini, Monica; Costanzini, Sofia; Teggi, Sergio

doi:10.1007/s10654-023-01009-0

Cited by 6 publications

(2 citation statements)

References 47 publications

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“…A wide number of studies evaluated air pollution and childhood cancer risk by assessing whether living nearby heavy-traffic roads or proximity to industrial and urban sites is associated with an increased cancer risk. Numerous studies have found positive associations not only with leukemia, but also with CNS cancer, neuroblastoma, Wilms tumor, and bone cancer, among other cancers ( Table 2 ) [ 13 , 14 , 16 , 24 , 29 , 30 , 31 , 32 , 34 , 37 , 43 , 46 , 54 , 61 ]. However, other studies have found mild or negative associations [ 12 , 16 , 21 , 25 , 39 , 45 , 60 , 185 ].…”

Section: Discussionmentioning

confidence: 99%

Environmental Pollution and Risk of Childhood Cancer: A Scoping Review of Evidence from the Last Decade

Navarrete-Meneses,

Salas-Labadía,

Gómez-Chávez

et al. 2024

IJMS

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The long-term effects of environmental pollution have been of concern as several pollutants are carcinogenic, potentially inducing a variety of cancers, including childhood cancer, which is a leading cause of death around the world and, thus, is a public health issue. The present scoping review aimed to update and summarize the available literature to detect specific environmental pollutants and their association with certain types of childhood cancer. Studies published from 2013 to 2023 regarding environmental pollution and childhood cancer were retrieved from the PubMed database. A total of 174 studies were eligible for this review and were analyzed. Our search strategy brought up most of the articles that evaluated air pollution (29%) and pesticides (28%). Indoor exposure to chemicals (11%), alcohol and tobacco use during pregnancy (16%), electromagnetic fields (12%), and radon (4%) were the subjects of less research. We found a particularly high percentage of positive associations between prenatal and postnatal exposure to indoor (84%) and outdoor (79%) air pollution, as well as to pesticides (82%), and childhood cancer. Positive associations were found between leukemia and pesticides and air pollution (33% and 27%); CNS tumors and neuroblastoma and pesticides (53% and 43%); and Wilms tumor and other rare cancers were found in association with air pollution (50%). Indoor air pollution was mostly reported in studies assessing several types of cancer (26%). Further studies are needed to investigate the mechanisms underlying the potential associations between indoor/outdoor air pollution and pesticide exposure with childhood cancer risk as more preventable measures could be taken.

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Section: Discussionmentioning

confidence: 99%

Environmental Pollution and Risk of Childhood Cancer: A Scoping Review of Evidence from the Last Decade

Navarrete-Meneses,

Salas-Labadía,

Gómez-Chávez

et al. 2024

IJMS

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“…In addition, certain behaviors, such as pica (placing hands and objects in one's mouth) and playing outside, increase children's odds of exposure (4). Regarding exposures in urban environments, residential proximity to petrol stations and industrial sites and exposure to mixtures of benzene, particulate matter ≤2.5 µm (PM 2.5 ), and polycyclic aromatic hydrocarbons (PAHs) from traffic emission are related to high risk of ALL (15)(16)(17)(18).…”

Section: Introductionmentioning

confidence: 99%

Childhood acute lymphoblastic leukemia survival and spatial analysis of socio-environmental risks in Mexico

Calderon-Hernandez,

Jarquin-Yañez,

Reyes-Arreguin

et al. 2023

Front. Oncol.

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BackgroundAcute lymphoblastic leukemia (ALL) etiology remains largely unknown; incidence patterns by age, sex, and geographical distribution suggest a potential environmental role.AimTo identify ALL clusters from four contrasting urban areas of Mexico and to characterize the sources of environmental carcinogens.MethodsHospital-based ALL cases (n = 443) diagnosed in children <19 years old from the Metropolitan Zones of Merida and San Luis Potosi, the State of Mexico, and Tijuana were analyzed (2015–2020). ALL cases were coded according to the International Classification of Diseases for Oncology. ALL clusters were identified by Kernel Density, and excess risk was estimated. Data of particulate matter ≤2.5 µm (PM2.5) concentrations measured by community-monitoring stations were analyzed. Geocoded datasets of benzene, polycyclic aromatic hydrocarbons, and PM2.5 sources were analyzed to characterize patterns of exposure in ALL clusters.ResultsThe survival rate for ALL ranged from 61.5% to 78.6%. Seven ALL clusters with excess risk (RR 1.4–2.3, p < 0.05) were identified. The carcinogen sources included artisanal brick kilns, gas stations, cement works, carpentry, paint, and chemical manufacturing establishments. PM2.5 levels ranged from 15 µg/m3 to 37 µg/m3 among study areas.ConclusionALL clusters were identified at the community level; the excess risk could be explained by small-scale carcinogen sources. The levels of PM2.5 in outdoor air ranged from 3 to 6 times above the World Health Organization (WHO) air quality guidelines. Healthcare providers must raise awareness of the increased risk of ALL in children living near sources of environmental carcinogens; cancer control and prevention strategies must be steered from a multi-sectoral and multi-action perspective to protect children’s health.

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DNMT1 regulates hypermethylation and silences hsa_circ_401351 in hydroquinone‐induced malignant TK6 cells

Han,

Meng,

Ling

et al. 2023

Environmental Toxicology

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BackgroundBenzene and its metabolite hydroquinone (HQ) are widely used in daily life, and long‐term exposure to benzene or HQ can induce acute myeloid leukemia (AML). Circular RNAs (circRNAs) are mostly produced by reverse splicing of gene exon mRNA precursors. The modulation of circRNA expression is connected to leukemia progression; however, the molecular mechanism is still unknown.Materials and methodsIn this study, the cells were divided into four groups: PBS control group (PBS‐TK6), TK6 malignantly transformed cells induced by 10.0 μmol/L HQ (HQ‐TK6), and HQ‐TK6 cells treated with 5 μmol/L 5‐AzaC (DNA methyltransferase inhibitor) for 24 h (HQ + 5‐AzaC). HQ‐TK6 cells were treated with 200 nmol/L TSA (histone deacetylation inhibitor) for 24 h (HQ + TSA). qRT–PCR was used to identify the differential hsa_circ_401351 expression between the four groups. We further determined the hsa_circ_401351 promoter methylation level with methylation‐specific PCR. DNMT1 and DNMT3b were knocked down by CRISPR/Cas9 to elucidate the specific molecular mechanism of hsa_circ_401351 in HQ‐TK6 cells. CCK‐8 and flow cytometry detected cell proliferation and apoptosis, respectively, after hsa_circ_401351 was overexpressed in HQ‐TK6 cells.ResultsCompared with the PBS‐TK6 group, the expression of hsa_circ_401351 was found to be lower in the HQ‐TK6 group. Nevertheless, treatment with 5‐AzaC or TSA increased hsa_circ_401351 expression, with the upregulation being more pronounced in the TSA group. The expression of hsa_circ_401351 in the DNMT1 knockdown group was dramatically increased by 50% compared to that in the control group, and the DNA methylation level of the hsa_circ_401351 promoter region was decreased. When hsa_circ_401351 was overexpressed, HQ‐TK6 cell proliferation was significantly slowed after 48 h compared with the control group. Flow cytometry showed that cells were mainly arrested in G1 phase, and apoptosis was significantly enhanced. Similarly, qRT–PCR and Western blot data showed significant reductions in Caspase‐3 mRNA and protein production, and Bcl‐2 mRNA levels were also elevated.ConclusionsOverall, our research showed that elevated DNMT1 expression in HQ‐TK6 cells increased methylation levels and decreased expression of the hsa_circ_401351 promoter region, limiting its ability to suppress HQ‐TK6 cell growth and enhance apoptosis.

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Residential proximity to petrol stations and risk of childhood leukemia

Cited by 6 publications

References 47 publications

Environmental Pollution and Risk of Childhood Cancer: A Scoping Review of Evidence from the Last Decade

Environmental Pollution and Risk of Childhood Cancer: A Scoping Review of Evidence from the Last Decade

Childhood acute lymphoblastic leukemia survival and spatial analysis of socio-environmental risks in Mexico

DNMT1 regulates hypermethylation and silences hsa_circ_401351 in hydroquinone‐induced malignant TK6 cells

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