HPV16 played a major role in the development of ≥CIN3 irrespective of age, supporting the identification of HPV16 in primary screening for all women. Identification of HPV18 is also warranted, given its significant contribution to AIS and cancer. Identification of non-16/18 genotypes as a pool should provide sufficient information for screening.

BackgroundFew 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.ObjectivesOur goal was to examine rates of lower respiratory illnesses in preschool children in relation to ambient particles and hydrocarbons.MethodsAir monitoring for particulate matter < 2.5 μm in diameter (PM2.5) 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.ResultsAfter 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/m3 PAHs and of 25 μg/m3 PM2.5 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.ConclusionAmbient 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.

Effects of air pollution on morbidity and mortality may be mediated by alterations in immune competence. In this study we examined short-term associations of air pollution exposures with lymphocyte immunophenotypes in cord blood among 1,397 deliveries in two districts of the Czech Republic. We measured fine particulate matter < 2.5 μm in diameter (PM2.5) and 12 polycyclic aromatic hydrocarbons (PAHs) in 24-hr samples collected by versatile air pollution samplers. Cord blood samples were analyzed using a FACSort flow cytometer to determine phenotypes of CD3+ T-lymphocytes and their subsets CD4+ and CD8+, CD19+ B-lymphocytes, and natural killer cells. The mothers were interviewed regarding sociodemographic and lifestyle factors, and medical records were abstracted for obstetric, labor and delivery characteristics. During the period 1994 to 1998, the mean daily ambient concentration of PM2.5 was 24.8 μg/m3 and that of PAHs was 63.5 ng/m3. In multiple linear regression models adjusted for temperature, season, and other covariates, average PAH or PM2.5 levels during the 14 days before birth were associated with decreases in T-lymphocyte phenotype fractions (i.e., CD3+ CD4+, and CD8+), and a clear increase in the B-lymphocyte (CD19+) fraction. For a 100-ng/m3 increase in PAHs, which represented approximately two standard deviations, the percentage decrease was −3.3% [95% confidence interval (CI), −5.6 to −1.0%] for CD3+, −3.1% (95% CI, −4.9 to −1.3%) for CD4+, and −1.0% (95% CI, −1.8 to −0.2%) for CD8+ cells. The corresponding increase in the CD19+ cell proportion was 1.7% (95% CI, 0.4 to 3.0%). Associations were similar but slightly weaker for PM2.5. Ambient air pollution may influence the relative distribution of lymphocyte immunophenotypes of the fetus.

The objective of this study was to analyze the mechanisms by which exposure to ambient air pollutants influences respiratory health may include altered prenatal immune development. To analyze associations between elevated cord serum Immunoglobulin E (IgE) levels and maternal air pollution exposure during each month of gestation. Total cord serum IgE was determined by the CAP system and mothers' total IgE levels by nephelometry for 459 births in the Czech Republic from May 1994 to mid-January 1997. Concentrations of polycyclic aromatic hydrocarbons (PAHs) and particulate matter <2.5 microns in diameter (PM(2.5) ) were measured in ambient air, and arithmetic means were calculated for each gestational month. Log binomial regression models were used to estimate prevalence ratios (PR) for elevated cord serum IgE (≥0.9 IU/ml) adjusting for district of residence, year of birth, and in further models, for maternal IgE (a surrogate for atopy) and gestational season. Heterogeneity by maternal atopy status was evaluated for associations of air pollution and of cigarette smoke. In adjusted models, PAH and PM(2.5) exposures in the second month of gestation were each associated with a lower prevalence of elevated cord serum IgE. For an average increase of 100 ng/m(3) of PAHs, the PR was 0.69 (95% confidence interval (CI): 0.50, 0.95); for 25 μg/m(3) increase in PM(2.5) , the PR was 0.77 (95% CI: 0.55, 1.07). Conversely, exposures later in gestation were associated with a higher prevalence of elevated cord IgE: in the fifth month, the PR for PAH exposure was 1.64 (95% CI: 1.29, 2.08), while for PM(2.5) in the sixth month, it was 1.66 (95% CI: 1.30, 2.13). In analyses stratified by maternal atopy, air pollutants were associated with altered cord serum IgE only among neonates with non-atopic mothers. Similarly, an association of cigarette smoke with elevated cord serum IgE was found only in non-atopic mothers. PAHs and PM(2.5) , constituents of both ambient air pollution and cigarette smoke, appear to influence fetal immune development, particularly among infants whose mothers are not atopic.

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