Bulky dna adducts in cord blood, maternal fruit-and-vegetable consumption, and birth weight in a European mother-child study (NewGeneris).

BACKGROUND: Tobacco-smoke, airborne, and dietary exposures to polycyclic aromatic hydrocarbons (PAHs) have been associated with reduced prenatal growth. Evidence from biomarker-based studies of low-exposed populations is limited. Bulky DNA adducts in cord blood reflect the prenatal effective dose to several genotoxic agents including PAHs. OBJECTIVES: We estimated the association between bulky DNA adduct levels and birth weight in a multicenter study and examined modification of this association by maternal intake of fruits and vegetables during pregnancy. METHODS: Pregnant women from Denmark, England, Greece, Norway, and Spain were recruited in 2006-2010. Adduct levels were measured by the 32P-postlabeling technique in white blood cells from 229 mothers and 612 newborns. Maternal diet was examined through questionnaires. RESULTS: Adduct levels in maternal and cord blood samples were similar and positively correlated (median, 12.1 vs. 11.4 adducts in 108 nucleotides; Spearman rank correlation coefficient = 0.66, p < 0.001). Cord blood adduct levels were negatively associated with birth weight, with an estimated difference in mean birth weight of -129 g (95% CI: -233, -25 g) for infants in the highest versus lowest tertile of adducts. The negative association with birth weight was limited to births in Norway, Denmark, and England, the countries with the lowest adduct levels, and was more pronounced in births to mothers with low intake of fruits and vegetables (-248 g; 95% CI: -405, -92 g) compared with those with high intake (-58 g; 95% CI: -206, 90 g). CONCLUSIONS: Maternal exposure to genotoxic agents that induce the formation of bulky DNA adducts may affect intrauterine growth. Maternal fruit and vegetable consumption may be protective.

Persistent respiratory symptoms in clean-up workers 5 years after the Prestige oil spill.

OBJECTIVES: Fishermen who had participated in clean-up activities of the Prestige oil spill showed an excess risk of respiratory symptoms 1-2 years later, but the long-term persistence of these health effects is unclear. The aim of this study was to evaluate the persistence of these respiratory symptoms 5 years after clean-up work. METHODS: Subgroups of 501 fishermen who had been exposed to clean-up work and 177 non-exposed individuals were re-interviewed by telephone in 2008, including the same symptom questions as in the initial survey. Associations between participation in clean-up work and respiratory symptoms were assessed using log-binomial and multinomial regression analyses adjusting for sex, age and smoking. RESULTS: Information from 466 exposed (93%) and 156 non-exposed (88%) fishermen was obtained. The prevalence of lower respiratory tract symptoms (including wheeze, shortness of breath, cough and phlegm) had slightly decreased in both groups, but remained higher among the exposed (RR 1.4, 95% CI 1.1 to 1.9). The risk of having persistent respiratory symptoms (reported both at baseline and at follow-up) increased with the degree of exposure: RR ratio 1.7 (95% CI 0.9 to 3.1) and 3.3 (95% CI 1.8 to 6.2) for moderately and highly exposed, respectively, when compared with those without any symptoms. Findings for nasal symptoms and for respiratory medication usage were similar. CONCLUSIONS: Participation in clean-up activities of oil spills may result in respiratory symptoms that persist up to 5 years after exposure. Guidelines for preventive measures and a continued surveillance of clean-up workers of oil spills are necessary.

Genotoxic effects in swimmers exposed to disinfection by-products in indoor swimming pools.

BACKGROUND: Exposure to disinfection by-products (DBPs) in drinking water has been associated with cancer risk. A recent study (Villanueva et al. 2007; Am J Epidemiol 165:148-156) found an increased bladder cancer risk among subjects attending swimming pools relative to those not attending. OBJECTIVES: We evaluated adults who swam in chlorinated pools to determine whether exposure to DBPs in pool water is associated with biomarkers of genotoxicity. METHODS: We collected blood, urine, and exhaled air samples from 49 nonsmoking adult volunteers before and after they swam for 40 min in an indoor chlorinated pool. We estimated associations between the concentrations of four trihalomethanes (THMs) in exhaled breath and changes in micronuclei (MN) and DNA damage (comet assay) in peripheral blood lymphocytes before and 1 hr after swimming; urine mutagenicity (Ames assay) before and 2 hr after swimming; and MN in exfoliated urothelial cells before and 2 weeks after swimming. We also estimated associations and interactions with polymorphisms in genes related to DNA repair or to DBP metabolism. RESULTS: After swimming, the total concentration of the four THMs in exhaled breath was seven times higher than before swimming. The change in the frequency of micronucleated lymphocytes after swimming increased in association with higher exhaled concentrations of the brominated THMs (p = 0.03 for bromodichloromethane, p = 0.05 for chlorodibromomethane, p = 0.01 for bromoform) but not chloroform. Swimming was not associated with DNA damage detectable by the comet assay. Urine mutagenicity increased significantly after swimming, in association with the higher concentration of exhaled bromoform (p = 0.004). We found no significant associations with changes in micronucleated urothelial cells. CONCLUSIONS: Our findings support potential genotoxic effects of exposure to DBPs from swimming pools. The positive health effects gained by swimming could be increased by reducing the potential health risks of pool water.