Malondialdehyde-deoxyguanosine and bulky DNA adducts in schoolchildren resident in the proximity of the Sarroch industrial estate on Sardinia Island, Italy

Abstract

Air quality is a primary environmental concern in highly industrialised areas, with potential health effects in children residing nearby. The Sarroch industrial estate in Cagliari province, Sardinia Island, Italy, hosts the world's largest power plant and the second largest European oil refinery and petrochemical park. This industrial estate produces a complex mixture of air pollutants, including benzene, heavy metals and polycyclic aromatic hydrocarbons. Thus, we conducted a cross-sectional study to evaluate the prevalence of malondialdehyde-deoxyguanosine adducts in the nasal epithelium of 75 representative children, aged 6-14 years, attending primary and secondary schools in Sarroch in comparison with 73 rural controls. Additionally, the levels of bulky DNA adducts were analysed in a subset of 62 study children. DNA damage was measured by (32)P-postlabelling methodologies. The air concentrations of benzene and ethyl benzene were measured in the school gardens of Sarroch and a rural village by diffusive samplers. Outdoor measurements were also performed in other Sarroch areas and in the proximity of the industrial estate. The outdoor levels of benzene and ethyl benzene were significantly higher in the school gardens of Sarroch than in the rural village. Higher concentrations were also found in other Sarroch areas and in the vicinity of the industrial park. The mean levels of malondialdehyde-deoxyguanosine adducts per 10(8) normal nucleotides ± standard error (SE) were 74.6±9.1 and 34.1±4.4 in the children from Sarroch and the rural village, respectively. The mean ratio was 2.53, 95% confidence interval (CI): 1.71-2.89, P < 0.001, versus rural controls. Similarly, the levels of bulky DNA adducts per 10(8) normal nucleotides ± SE were 2.9±0.4 and 1.6±0.2 in the schoolchildren from Sarroch and the rural village, respectively. The means ratio was 1.90, 95% CI: 1.25-2.89, P = 0.003 versus rural controls. Our study indicates that children residing near the industrial estate have a significant increment of DNA damage.

Formaldehyde-induced toxicity in the nasal epithelia of workers of a plastic laminate plant

“…Since the molecular mechanisms by which FA causes nasopharyngeal cancer are not completely understood, 5 we have conducted a mechanistic study to evaluate the association between M 1 dG adducts, a biomarker of oxidative stress and lipid peroxidation, [21][22][23][24][25] with personal air FA exposure in the nasal epithelia of plastic laminate plant workers using 32 Ppost-labelling and GC-MS techniques. Our aim was to study the mechanisms of FA-induced toxicity in the portal-of-entry of air FA as well as in the target site for FA-induced nasal carcinogenesis.…”

“…48 Nasal epithelia is commonly represented by 75% of columnar surface epithelium, 14% of other epithelial cells, 11% of neutrophils, 0.07% of eosinophils and 0.2% lymphocytes. Apart from the potential value of the nasal epithelial cells for the prediction of cancer risk of the respiratory tract, 16,27 the use of nasal epithelia may allow mechanistic studies of various carcinogens, including those contained in tobacco smoke, 16,39 industrial air pollution, [20][21][22]28 and hair-dyeing. 49 Additionally, the patterns of Phase I enzymes that have an important role in the production of ROS during the metabolism of a number of carcinogens 50 are qualitatively different in the respiratory tract than in other tissues.…”

“…13,14 DNA mutations, as well as altered patterns of DNA methylation are important hallmarks in carcinogenesis, and clinical studies indeed showed that enhanced levels of M 1 dG adducts may be linked to cancer development and tumor progression. [15][16][17][18][19] Exocyclic M 1 dG adducts reflect also the extent of various carcinogen exposures, [20][21][22] including FA in pathology wards. 23 In particular, we have found that working in the reduction rooms and being exposed to FA at levels greater than 66 μg m −3 was associated with increased generation of M 1 dG adducts.…”

“…23 In the present study, we have examined the mechanisms of FA-induced toxicity in the nasal epithelia of plastic laminate plant workers, hence in the target site for FA-induced nasal carcinogenesis. Our approach consisted of conducting a crosssectional study aimed to compare the frequency of M 1 dG adducts, a biomarker of oxidative stress and lipid peroxidation, [21][22][23][24][25] in the nasal epithelia of FA workers with respect to controls. DNA damage measurement analyzing exfoliated nasal epithelial cells is considered a promising approach for the detection of genotoxic compounds in the occupational setting, 16,20,21,[26][27][28] because these cells may be obtained easily by nasal brushing, a minimal invasive method.…”

“…Our approach consisted of conducting a crosssectional study aimed to compare the frequency of M 1 dG adducts, a biomarker of oxidative stress and lipid peroxidation, [21][22][23][24][25] in the nasal epithelia of FA workers with respect to controls. DNA damage measurement analyzing exfoliated nasal epithelial cells is considered a promising approach for the detection of genotoxic compounds in the occupational setting, 16,20,21,[26][27][28] because these cells may be obtained easily by nasal brushing, a minimal invasive method. 16 M 1 dG adducts have been examined in the nasal epithelial cells using the 32 P-DNA post-labeling technique, 25,[29][30][31][32] whereas the indoor levels of FA have been measured by using passive personal air samplers using the gas-chromatography mass-spectrometry (GC-MS) technique.…”