Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants that are generated by the incomplete combustion of organic materials. The main anthropogenic sources of PAHs are the combustion of solid fuels for heating purposes, illegal waste incineration, road transport and industries based on fossil fuels. PAHs can easily enter the body because they are present in all elements of the environment, including water, soil, air, and food. Due to their ubiquitous presence, PAHs, may exert a harmful effect on human health. Assessing PAH exposure through biomonitoring mostly involve techniques to measure the concentration of 1-hydroxypyrene in human urine. Nevertheless, through recent progress in analytical techniques, other common metabolites of PAHs in human biospecimens can be detected. A scientific literature search was conducted to determine which hydroxy derivatives of PAHs are markers of PAHs exposure and to reveal the leading sources of these compounds. Techniques for analyzing biological samples to identify OH-PAHs are also discussed. The most frequently determined OH-PAH in human urine is 1-hydroxypyrene, the concentration of which reaches up to a dozen ng/L in urine. Apart from this compound, the most frequently determined biomarkers were naphthalene and fluorene metabolites. The highest concentrations of 1- and 2-hydroxynaphthalene, as well as 2-hydroxyfluorene, are associated with occupational exposure and reach approximately 30 ng/L in urine. High molecular weight PAH metabolites have been identified in only a few studies. To date, PAH metabolites in feces have been analyzed only in animal models for PAH exposure. The most frequently used analytical method is HPLC-FLD. However, compared to liquid chromatography, the LOD for gas chromatography methods is at least one order of magnitude lower. The hydroxy derivatives naphthalene and fluorene may also serve as indicators of PAH exposure.
An unfavorable trend of increasing rates of colorectal cancer has been observed across modern societies. In general, dietary factors are understood to be responsible for up to 70% of the disease’s incidence, though there are still many inconsistencies regarding the impact of specific dietary items. Among the dietary minerals, calcium intake may play a crucial role in the prevention. The purpose of this study was to assess the effect of intake of higher levels of dietary calcium on the risk of developing of colorectal cancer, and to evaluate dose dependent effect and to investigate possible effect modification.
Objectives: The aim of the study was to assess the relative validity of a semi-quantitative FFQ (SFFQ) which measures the usual dietary intake of 3-year-old children.Design: The children's daily dietary intake was measured using the SFFQ. The average intake of three 24 h dietary recalls (24hDR) was calculated as a reference method. Wilcoxon's rank test and Spearman's rank-correlation coefficient were used to compare nutrient intakes assessed by both methods. The level of agreement between the SFFQ and the repeated 24hDR was determined by the Bland–Altman method. To assess the agreement in quartile distribution, the weighted kappa coefficient (κw) was used.Setting: Krakow, Poland.Subjects: One hundred and forty-three 3-year-old children and their mothers, participants of a prospective cohort study.Results: Overall, the SFFQ overestimated energy and nutrient intakes compared with the repeated 24hDR. The median correlation coefficient for energy and nutrient intakes was 0·456, with higher results for Ca, P and riboflavin. Although theκwvalue showed only slight to fair agreement between the two methods, about 75 % of the children were classified into the same or adjacent quartile and the level of agreement assessed by the Bland–Altman method for most of the nutrients investigated was good.Conclusions: The study indicated that the SFFQ might be a useful tool to assess dietary intakes of nutrients by small children, especially for ranking them according their nutrient intake.
1 January 2008 in Annals of Nutrition and Metabolism
Background/Aims: Current epidemiologic studies investigating the effect of fish intake on colorectal cancer (CRC) risk are scarce. Therefore, the aim of this study was to elucidate the relationship between fish consumption and CRC risk. Methods: This hospital-based case-control study was performed in 548 CRC patients (Surgery Clinic, University Hospital in Krakow, Poland) between November 2000 and May 2008. Histological findings, information on anatomic location and stage of cancer were available for all the patients enrolled in this study. The control group consisted of 745 patients of the same hospital with no history of cancer admitted for treatment of non-neoplastic conditions. During the 5-year study period, the food frequency questionnaire used focused on the reference period that was defined as 1–5 years prior to CRC diagnosis for the CRC cases and the date of hospital admission for the controls. Results: Thecrude odds ratio (OR) was inversely related to fish consumption (z for trend in quartiles of intake = –2.31, p = 0.021; OR = 0.89; 95% confidence interval, CI: 0.81–0.98). The risk of CRC increased with intake of stewed or cooked meat (z for trend in quartiles of intake = 2.14; p = 0.032; OR = 1.11; 95% CI: 1.01–1.23). The adjusted OR showed a significant reduction in CRC already at the moderate fish intake of one or two servings per week (OR = 0.70; 95% CI: 0.51–0.94), but it was even lower at higher fish intake (OR = 0.56; 95% CI: 0.39–0.86). All multivariate statistical models employed in the analysis considered potential confounders, such as demographic characteristics of subjects, body mass index, smoking status, leisure time physical activity, energy consumption and intake of meat products. Conclusions: The study results indicate that increased fish intake may have a preventive effect on CRC and modulate the effect of meat consumption. To our knowledge, this is the first large epidemiologic study on dietary habits and CRC incidence in Eastern Europe.
30 January 2008 in Annals of Nutrition and Metabolism
The purpose of the study was to test the hypothesis whether infants with higher prenatal exposure to fine particles (PM2.5) are at greater risk of developing respiratory symptoms and whether fish consumption in pregnancy may modulate the effect. The study was carried out in a cohort of 465 newborns in Krakow (Poland) who have been followed over the first 2 years of life and for whom data on the occurrence of respiratory symptoms and measurements of personal air monitoring in the second trimester of pregnancy were available. The incidence risk ratio (IRR) of respiratory symptoms due to prenatal PM2.5 exposure were adjusted for potential confounders (gender of child, breastfeeding, parity, maternal atopy, maternal education as a proxy for the socio-economic status, exposure to postnatal environmental tobacco smoke (ETS), and moulds in households) in the generalized estimating equations (GEE) statistical models. The adjusted risk of coughing was associated significantly with PM2.5 level (IRR = 2.51; 95% CI: 1.77–3.58), moulds in the household, parity, maternal atopy and postnatal ETS, but was lower in girls, and in infants whose mothers consumed more fish in pregnancy (IRR = 0.85; 95% CI: 0.79–0.91). The risk of wheezing was also correlated significantly with the prenatal exposure to PM2.5 (IRR = 1.36; 95% CI: 1.29–1.43) but also with the presence of moulds in homes, parity, maternal atopy and postnatal ETS. The occurrence of wheezing was associated inversely with the gender of child, gestational age, and fish consumption in pregnancy (IRR = 0.97; 95% CI: 0.95–0.99). Similarly, the risk of difficult (puffy) breathing increased with prenatal exposure to PM2.5 (IRR = 1.18; 95% CI: 1.12–1.25) moulds, maternal atopy, and parity. The symptom occurrence was lower in girls and associated inversely with the gestational age, and fish consumption in pregnancy (IRR = 0.94; 95% CI: 0.92–0.97). The results of the study support the hypothesis that fish consumption in pregnancy may mitigate the harmful effect of prenatal or perinatal exposure to components of PM2.5 resulting in an increased burden of respiratory infections among infants.