Outdoor formaldehyde and N[O.sub.2] exposures and markers of genotoxicity in children living near chipboard industries

• Published in: Environmental health perspectives 2014-06, Vol.122 (6), p.639
• Main Authors: Marcon, Alessandro, Fracasso, Maria Enrica, Marchetti, Pierpaolo, Doria, Denise, Girardi, Paolo, Guarda, Linda, Pesce, Giancarlo, Pironi, Vanda, Ricci, Paolo, de Marco, Roberto
• Format: Article
• Language: English
• Subjects: Cells; DNA damage; Environmental aspects; Formaldehyde; Genetic aspects; Health aspects; Nitrogen dioxide; Physiological aspects
• ISSN: 0091-6765; 1552-9924
• DOI: 10.1289/ehp.1307259

BACKGROUND: Industrial air pollution is a public health hazard. Previous evidence documented increased respiratory symptoms and hospitalizations in children who live near the factories in the largest chipboard manufacturing district in Italy (Viadana). OBJECTIVES: We evaluated the association of outdoor exposure to formaldehyde and nitrogen dioxide (N[O.sub.2]) with markers of early genotoxic damage in oral mucosa cells of randomly selected children (6-12 years of age) living in Viadana. METHODS: In 2010-2011, DNA strand breaks and nuclear abnormalities were evaluated in exfoliated buccal cells by the comet and micronucleus assays, respectively, and formaldehyde and N[O.sub.2] were monitored by passive sampling. Annual exposure estimates to pollutants were assigned to children's houses by spatial interpolation. RESULTS: Of 656 children, 413 (63%) participated. Children living near (< 2 km) the chipboard industries had the highest average exposure to formaldehyde and N[O.sub.2] (p < 0.001). A 1-SD increase in formaldehyde (0.20 µg/[m.sup.3]) was associated with a 0.13% (95% CI: 0.03, 0.22%) higher comet tail intensity, a 0.007 (95% CI: 0.001, 0.012) higher tail moment, and a 12% relative increase [relative risk (RR) = 1.12; 95% CI: 1.02, 1.23] in nuclear buds. A 1-SD N[O.sub.2] increase (2.13 µg/[m.sup.3]) was associated with a 0.13% (95% CI: 0.07, 0.19%) increase in binucleated cells and a 16% relative increase (RR = 1.16; 95% CI: 1.06, 1.26) in nuclear buds. CONCLUSIONS: Exposure to pollutants was associated with markers of genotoxicity in exfoliated buccal cells of children living in a region with chipboard industries. These findings, combined with previously reported associations between chipboard industrial activities and respiratory outcomes in children, add to concerns about potential adverse effects of industry-related exposures in the Viadana district.