Prenatal Exposure to Perfluoroalkyl Substances and Body Fatness in Girls.

BACKGROUND: Perfluoroalkyl substances (PFASs) are used in surface coatings that resist stains, grease, and water. METHODS: The association between in utero PFAS exposure and girls' body fatness at age 9 was analyzed in The Avon Longitudinal Study of Parents and Children (UK). Maternal serum [median 15 weeks: interquartile range (IQR) 10 and 28 weeks of gestation] was analyzed for perfluorooctane sulfonate (PFOS), perfluorooctanoate (PFOA), perfluorohexane sulfonate (PFHxS), and perfluorononanoate (PFNA). Body composition was measured by dual X-ray emission absorptiometry, and percent total body fat (%BF) was calculated. Associations between PFASs and body fatness were modeled by multivariable linear regression. RESULTS: Among 359 girls, median (IQR) %BF was 27.5 (IQR 21.7-34.6). Median (IQR) concentrations (all ng/mL) were 3.7 (2.9-4.8) for PFOA, 19.8 (15.0-25.3) for PFOS, 1.6 (1.3-2.2) for PFHxS, and 0.5 (0.4-0.7) for PFNA. Maternal PFAS concentrations were not significantly associated with daughters' total %BF overall. Mothers' educational status modified associations for PFOA and PFOS with %BF (P-interactions: 0.005 and 0.02, respectively). %BF was higher [1.4%; 95% confidence interval (95% CI): 0.3 to 2.5] for each one unit (ng/mL) higher PFOA among girls with mothers in the middle education group, but lower (-0.6%; 95% CI: -1.12 to -0.04) for the corresponding comparison among girls with mothers with the highest education. %BF was lower (-0.2%; 95% CI: -0.3 to -0.1) for each one unit higher PFOS among girls with the most educated mothers. CONCLUSIONS: Prenatal exposure to PFOA and PFOS was associated with girls' %BF within some strata of maternal education status. PFHxS and PFNA were not associated with %BF.

Case-control study of breast cancer and exposure to synthetic environmental chemicals among Alaska Native women.

BACKGROUND: Exposure to environmental chemicals may impair endocrine system function. Alaska Native (AN) women may be at higher risk of exposure to these endocrine disrupting chemicals, which may contribute to breast cancer in this population. OBJECTIVE: To measure the association between exposure to select environmental chemicals and breast cancer among AN women. DESIGN: A case-control study of 170 women (75 cases, 95 controls) recruited from the AN Medical Center from 1999 to 2002. Participants provided urine and serum samples. Serum was analyzed for 9 persistent pesticides, 34 polychlorinated biphenyl (PCB) congeners, and 8 polybrominated diethyl ether (PBDE) congeners. Urine was analyzed for 10 phthalate metabolites. We calculated geometric means (GM) and compared cases and controls using logistic regression. RESULTS: Serum concentrations of most pesticides and 3 indicator PCB congeners (PCB-138/158; PCB-153, PCB-180) were lower in case women than controls. BDE-47 was significantly higher in case women (GM=38.8 ng/g lipid) than controls (GM=25.1 ng/g lipid) (p=0.04). Persistent pesticides, PCBs, and most phthalate metabolites were not associated with case status in univariate logistic regression. The odds of being a case were higher for those with urinary mono-(2-ethylhexyl) phthalate (MEHP) concentrations that were above the median; this relationship was seen in both univariate (OR 2.16, 95% CI 1.16-4.05, p=0.02) and multivariable (OR 2.43, 95% CI 1.13-5.25, p=0.02) logistic regression. Women with oestrogen receptor (ER)-/progesterone receptor (PR)-tumour types tended to have higher concentrations of persistent pesticides than did ER+/PR+ women, although these differences were not statistically significant. CONCLUSIONS: Exposure to the parent compound of the phthalate metabolite MEHP may be associated with breast cancer. However, our study is limited by small sample size and an inability to control for the confounding effects of body mass index. The association between BDE-47 and breast cancer warrants further investigation.

Timing of maturation and predictors of Tanner stage transitions in boys enrolled in a contemporary British cohort.

This study describes the timing of puberty in 8- to 14-year-old boys enrolled in the Avon Longitudinal Study of Parents and Children (ALSPAC) and identifies factors associated with earlier achievement of advanced pubic hair stages. Women were enrolled during pregnancy and their offspring were followed prospectively. We analysed self-reported pubic hair Tanner staging collected annually. We used survival models to estimate median age of attainment of pubic hair stage >1, stage >2 and stage >3 of pubic hair development. We also constructed multivariable logistic regression models to identify factors associated with earlier achievement of pubic hair stages. Approximately 5% of the boys reported Tanner pubic hair stage >1 at age 8; 99% of boys were at stage >1 by age 14. The estimated median ages of entry into stages of pubic hair development were 11.4 years [95% confidence interval (CI) 11.3, 11.4] for stage >1, 12.7 years [95% CI 12.7, 12.8] for stage >2 and 13.5 years [95% CI 13.5, 13.6] for stage >3. Predictors of younger age at Tanner stage >1 included low birthweight, younger maternal age at delivery and being taller at age 8. Associations were found between younger age at attainment of stage >2 and gestational diabetes and taller or heavier body size at age 8. Being taller or heavier at age 8 also predicted younger age at Tanner stage >3. The results give added support to the strong influence of pre-adolescent body size on male pubertal development; the tallest and heaviest boys at 8 years achieved each stage earlier and the shortest boys later. Age at attainment of pubic hair Tanner stages in the ALSPAC cohort are similar to ages reported in other European studies that were conducted during overlapping time periods. This cohort will continue to be followed for maturational information until age 17.

Pesticide exposure resulting from treatment of lice infestation in school-aged children in Georgia.

OBJECTIVE: The objective of this study was to assess pesticide exposures in children being treated for head lice with either lindane or permethrin (exposed group) and children who did not have a lice infestation and thus were not being treated with chemicals for head lice or scabies (unexposed group). METHODS: In 2001, we enrolled 78 children aged 6-10 years old and collected baseline urine samples and demographic information from all the children. We subsequently collected post-exposure urine samples and questionnaire information about lice treatment from the 29 (37%) children (exposed children) who had been diagnosed and were being treated for head lice. Metabolites of the pesticides lindane and permethrin were measured in the samples. RESULTS: The mean age of exposed and unexposed children in the study population was 9.3 years and 8.5 years, respectively. Fourteen of the 29 exposed children used prescription lice treatments (i.e., lindane or malathion); 25 of the 29 exposed children used at least one over-the-counter permethrin treatment, either alone or in addition to prescription treatments. Exposed children in both counties had higher urinary pyrethroid metabolite levels in their post-exposure samples compared with their baseline samples. However this difference was only significant in Forsyth County children. CONCLUSIONS: The significantly increased post-exposure pyrethroid metabolite levels in the urine of Forsyth County children suggest that the children are exposed to pyrethroid insecticides through the use of lice shampoos.

Investigating childhood leukemia in Churchill County, Nevada.

BACKGROUND: Sixteen children diagnosed with acute leukemia between 1997 and 2002 lived in Churchill County, Nevada, at the time of or before their illness. Considering the county population and statewide cancer rate, fewer than two cases would be expected. OBJECTIVES: In March 2001, the Centers for Disease Control and Prevention led federal, state, and local agencies in a cross-sectional, case-comparison study to determine if ongoing environmental exposures posed a health risk to residents and to compare levels of contaminants in environmental and biologic samples collected from participating families. METHODS: Surveys with more than 500 variables were administered to 205 people in 69 families. Blood, urine, and cheek cell samples were collected and analyzed for 139 chemicals, eight viral markers, and several genetic polymorphisms. Air, water, soil, and dust samples were collected from almost 80 homes to measure more than 200 chemicals. RESULTS: The scope of this cancer cluster investigation exceeded any previous study of pediatric leukemia. Nonetheless, no exposure consistent with leukemia risk was identified. Overall, tungsten and arsenic levels in urine and water samples were significantly higher than national comparison values; however, levels were similar among case and comparison groups. CONCLUSIONS: Although the cases in this cancer cluster may in fact have a common etiology, their small number and the length of time between diagnosis and our exposure assessment lessen the ability to find an association between leukemia and environmental exposures. Given the limitations of individual cancer cluster investigations, it may prove more efficient to pool laboratory and questionnaire data from similar leukemia clusters.

Genetic studies of a cluster of acute lymphoblastic leukemia cases in Churchill County, Nevada.

OBJECTIVE: In a study to identify exposures associated with 15 cases of childhood leukemia, we found levels of tungsten, arsenic, and dichlorodiphenyldichloroethylene in participants to be higher than mean values reported in the National Report on Human Exposure to Environmental Chemicals. Because case and comparison families had similar levels of these contaminants, we conducted genetic studies to identify gene polymorphisms that might have made case children more susceptible than comparison children to effects of the exposures. DESIGN: We compared case with comparison children to determine whether differences existed in the frequency of polymorphic genes, including genes that code for enzymes in the folate and purine pathways. We also included discovery of polymorphic forms of genes that code for enzymes that are inhibited by tungsten: xanthine dehydrogenase, sulfite oxidase (SUOXgene), and aldehyde oxidase. PARTICIPANTS: Eleven case children were age- and sex-matched with 42 community comparison children for genetic analyses. Twenty parents of case children also contributed to the analyses. RESULTS: One bilalleleic gene locus in SUOX was significantly associated with either case or comparison status, depending on which alleles the child carried (without adjusting for multiple comparisons). CONCLUSIONS: Although genetic studies did not provide evidence that a common agent or genetic susceptibility factor caused the leukemias, the association between a SUOXgene locus and disease status in the presence of high tungsten and arsenic levels warrants further investigation. RELEVANCE: Although analyses of community clusters of cancer have rarely identified causes, these findings have generated hypotheses to be tested in subsequent studies.