Early childhood lower respiratory illness and air pollution.

BACKGROUND: Few studies of air pollutants address morbidity in preschool children. In this study we evaluated bronchitis in children from two Czech districts: Teplice, with high ambient air pollution, and Prachatice, characterized by lower exposures. OBJECTIVES: Our goal was to examine rates of lower respiratory illnesses in preschool children in relation to ambient particles and hydrocarbons. METHODS: Air monitoring for particulate matter < 2.5 microm in diameter (PM(2.5)) and polycyclic aromatic hydrocarbons (PAHs) was conducted daily, every third day, or every sixth day. Children born May 1994 through December 1998 were followed to 3 or 4.5 years of age to ascertain illness diagnoses. Mothers completed questionnaires at birth and at follow-up regarding demographic, lifestyle, reproductive, and home environmental factors. Longitudinal multivariate repeated-measures analysis was used to quantify rate ratios for bronchitis and for total lower respiratory illnesses in 1,133 children. RESULTS: After adjustment for season, temperature, and other covariates, bronchitis rates increased with rising pollutant concentrations. Below 2 years of age, increments in 30-day averages of 100 ng/m(3) PAHs and of 25 microg/m(3) PM(2.5) resulted in rate ratios (RRs) for bronchitis of 1.29 [95 % confidence interval (CI), 1.07-1.54] and 1.30 (95% CI, 1.08-1.58), respectively; from 2 to 4.5 years of age, these RRs were 1.56 (95% CI, 1.22-2.00) and 1.23 (95% CI, 0.94-1.62), respectively. CONCLUSION: Ambient PAHs and fine particles were associated with early-life susceptibility to bronchitis. Associations were stronger for longer pollutant-averaging periods and, among children > 2 years of age, for PAHs compared with fine particles. Preschool-age children may be particularly vulnerable to air pollution-induced illnesses.

The DNA repair gene XPD/ERCC2 polymorphisms Arg156Arg (exon 6) and Lys751Gln (exon 23) are closely associated.

In the context of a molecular epidemiology study dealing with the effects of individual genetic susceptibility on childhood respiratory morbidity, DNA repair genotypes for the XPD/ERCC2 gene in exon 6 (Arg156Arg) and exon 23 (Lys751Gln) have been analyzed by PCR/RFLP assays in DNA samples isolated from the fetal parts of placentas. The study was performed using a cohort of 729 children born in 1994-1998 in two districts of the Czech Republic. On the basis of these data, we tested the association between the two genotypes. The principal finding of this study is that the exon 6 and exon 23 polymorphisms in the XPD/ERCC2 gene are tightly associated, with persons who are homozygous CC in exon 23 being mostly (81%) homozygous CC in exon 6, and persons homozygous AA in exon 6 mostly (88%) homozygous AA in exon 23. This strong association may have serious consequences for the interpretation of cancer susceptibility and other molecular epidemiology studies dealing with the XPD6 and XPD23 genotypes, since the observed effects of the silent XPD6 polymorphism might be, in fact, the result of XPD23 polymorphism, which is connected with an amino acid substitution in the resulting XPD protein.

Maternal DDT exposures in relation to fetal and 5-year growth.

BACKGROUND: Dichlorodiphenyltrichloroethane (DDT) is an organochlorine pesticide still used in areas of the world where malaria vector control is needed. Few studies have examined in utero exposures to DDT in relation to fetal and early childhood growth in populations with substantial exposure to DDT. Furthermore, only a portion of these studies have investigated in utero exposures and growth during childhood. METHODS: To assess the role of in utero exposures to DDT on fetal and early childhood growth, we analyzed data from mothers and children who participated in the Child Health and Development Study (CHDS), a cohort study of 20,754 women and their pregnancies conducted in the San Francisco Bay area during the 1960s. We measured p,p'-DDE, o,p'-DDT, and p,p'-DDT concentrations from the stored sera of 399 women collected during pregnancy. Outcomes were measured at the child's birth and at 5 years of age. RESULTS: Maternal p,p'-DDE concentrations were considerable in this study, averaging 6.9 micrograms per gram lipid. After covariate adjustment, a small increase in gestational age was observed with increases in p,p'-DDT and o,p'-DDT, but there was no association with p,p'-DDE. At 5 years of age, an increase from the 25th to the 75th percentile in p,p'-DDE was related to a 2-mm increase in head circumference (95% confidence interval = 0 to 4). Overall effect sizes were small and imprecise. Furthermore, there was little evidence of specificity for a given outcome or exposure at either age. CONCLUSIONS: At the concentrations studied in this sample, DDT compounds did not appear to impair fetal or 5-year growth.