122 research outputs found
Self-Reported Chemicals Exposure, Beliefs About Disease Causation, and Risk of Breast Cancer in the Cape Cod Breast Cancer and Environment Study: A Case-Control Study
BACKGROUND: Household cleaning and pesticide products may contribute to breast cancer because many contain endocrine disrupting chemicals or mammary gland carcinogens. This population-based case-control study investigated whether use of household cleaners and pesticides increases breast cancer risk. METHODS: Participants were 787 Cape Cod, Massachusetts, women diagnosed with breast cancer between 1988 and 1995 and 721 controls. Telephone interviews asked about product use, beliefs about breast cancer etiology, and established and suspected breast cancer risk factors. To evaluate potential recall bias, we stratified product-use odds ratios by beliefs about whether chemicals and pollutants contribute to breast cancer; we compared these results with odds ratios for family history (which are less subject to recall bias) stratified by beliefs about heredity. RESULTS: Breast cancer risk increased two-fold in the highest compared with lowest quartile of self-reported combined cleaning product use (Adjusted OR = 2.1, 95% CI: 1.4, 3.3) and combined air freshener use (Adjusted OR = 1.9, 95% CI: 1.2, 3.0). Little association was observed with pesticide use. In stratified analyses, cleaning products odds ratios were more elevated among participants who believed pollutants contribute "a lot" to breast cancer and moved towards the null among the other participants. In comparison, the odds ratio for breast cancer and family history was markedly higher among women who believed that heredity contributes "a lot" (OR = 2.6, 95% CI: 1.9, 3.6) and not elevated among others (OR = 0.7, 95% CI: 0.5, 1.1). CONCLUSIONS: Results of this study suggest that cleaning product use contributes to increased breast cancer risk. However, results also highlight the difficulty of distinguishing in retrospective self-report studies between valid associations and the influence of recall bias. Recall bias may influence higher odds ratios for product use among participants who believed that chemicals and pollutants contribute to breast cancer. Alternatively, the influence of experience on beliefs is another explanation, illustrated by the protective odds ratio for family history among women who do not believe heredity contributes "a lot." Because exposure to chemicals from household cleaning products is a biologically plausible cause of breast cancer and avoidable, associations reported here should be further examined prospectively.Massachusetts Legislature; Massachusetts Department of Public Health; Susan S. Bailis Breast Cancer Research Fund at Silent Spring Institute; United States Centers for Disease Control and Prevention (R01 DP000218-01, 1H75EH000377-01
Fast Food: A Source of Exposure to Phthalates and Bisphenol A in a Nationally Representative Sample
Background: Certain phthalates and bisphenol A (BPA) are industrial chemicals widely used in consumer products that can adversely impact human health. Diet is hypothesized to be a major source of exposure but little is known about the impact of specific food sources. This study aims to investigate the association between fast food consumption with human exposure to high-molecular weight phthalates (di(2-ethylhexyl) phthalate (DEHP) and diisononyl phthalate (DINP)) and BPA, in 8876 participants, aged 6 to 85 years old, from the National Health and Nutrition Examination Survey (NHANES), 2003-2010.
Methodology: During the NHANES mobile exam, participants: 1) provided a spot urine sample which was measured for metabolites of DEHP, DINP, and BPA; and 2) completed a 24-hour dietary recall survey. We calculated kilocalorie intake of fast food from the dietary survey, and modeled fast food consumption in the prior 24-hours dichotomously and categorically as the percent of total daily calories (0%,
Results: The majority of study subjects had detectable levels of urinary phthalate and BPA metabolites in their urine. Those who had eaten fast food had significantly higher urinary metabolite levels of ΣDEHP [percent change (95%CI): 18.63% (10.38%, 27.50%)] and DINP [percent change (95%CI): 32.17% (20.04%, 45.52%)], but not BPA [percent change (95%CI): 2.36% (-2.59%, 7.56%)] compared to those who had not eaten fast food in adjusted models. For ΣDEHP and DINP, there was evidence of a positive dose-response effect (p for trend \u3c 0.0001). Meat and grain consumption were associated with ΣDEHP and DINP when adjusting for all food groups.
Discussion: Findings suggest that fast food consumption may be an important exposure source for DEHP and DINP, but not BPA, among the general population. Consistent with other studies that report high phthalate residues in high fat foods, our findings suggest that meat-centric meals may in part be responsible for this association. Further research should investigate which components of the fast food industry (production and storage, cooking process, packaging, etc.) contribute to this association
Association between Occupational Exposures to Informal Sector E-Waste and DNA Damage: A Systematic Review
Breastfeeding as a Predictor of Serum Concentrations of Per- and Polyfluorinated Alkyl Substances in Reproductive-aged Women and Children: A Rapid Systematic Review
Purpose of Review: Per- and polyfluorinated alkyl substances (PFASs) are synthetic chemicals widely detected in human serum, and at low levels in breast milk. We conducted a rapid systematic review on breastfeeding practices and serum concentrations of PFASs – specifically PFOS and PFOA - among reproductive-aged women and young children using the Navigation Guide systematic review methodology.
Recent Findings: We included 14 studies examining associations between breastfeeding and PFASs in infants/toddlers or pregnant/postnatal women. Breastfeeding was significantly associated with lower PFASs exposure among women and higher PFASs exposure among children. Summary: We concluded there was “sufficient” evidence supporting an association between breastfeeding and serum PFASs concentrations among women, and “limited” evidence of an association among children due to issues with sample size, confounding, and exposure assessment. These findings reinforce that lactation is an important excretion route of PFASs for women, and that breast milk may be an important exposure pathway for young children
Recent fast food consumption and bisphenol A and phthalates exposures among the U.S. population in NHANES, 2003-2010
Background: Phthalates and bisphenol A (BPA) are widely used industrial chemicals that may adversely impact human health. Human exposure is ubiquitous and can occur through diet, including consumption of processed or packaged food.
Objective: To examine associations between recent fast food intake and BPA and urinary metabolites of di(2-ethylhexyl) phthalate (ΣDEHPm) and diisononyl phthalate (DiNPm) among the US population.
Methods: We combined data on 8877 participants from the National Health and Nutrition Examination Survey (NHANES 2003-2010). Using 24-hour dietary recall data, we quantified: 1) fast food intake (percent of total energy intake (TEI) from fast food); 2) fast food-derived fat intake (percent of TEI from fat in fast food); and 3) fast food intake by food group (dairy, eggs, grains, meat, and other). We examined associations between dietary exposures and urinary chemical concentrations using multivariate linear regression.
Results: We observed evidence of a positive, dose–response relationship between fast food intake and exposure to phthalates (p-trend \u3c 0.0001) but not BPA; participants with high consumption (≥ 34.9% TEI from fast food) had 23.8% (95% CI: 11.9%, 36.9%) and 39.0% (95% CI: 21.9%, 58.5%) higher levels of ΣDEHPm and DiNPm, respectively, than nonconsumers. Fast food-derived fat intake was also positively associated with ΣDEHPm and DiNPm (p-trend \u3c 0.0001). After adjusting for other food groups, ΣDEHPm was associated with grain and other intake, and DiNPm was associated with meat and grain intake.
Conclusion: Fast food may be a source of exposure to DEHP and DiNP. These results, if confirmed, could inform individual and regulatory exposure reduction strategies
Environmental Chemicals in Pregnant Women in the United States: NHANES 2003–2004
BackgroundExposure to chemicals during fetal development can increase the risk of adverse health effects, and while biomonitoring studies suggest pregnant women are exposed to chemicals, little is known about the extent of multiple chemicals exposures among pregnant women in the United States.ObjectiveWe analyzed biomonitoring data from the National Health and Nutritional Examination Survey (NHANES) to characterize both individual and multiple chemical exposures in U.S. pregnant women.MethodsWe analyzed data for 163 chemical analytes in 12 chemical classes for subsamples of 268 pregnant women from NHANES 2003-2004, a nationally representative sample of the U.S. population. For each chemical analyte, we calculated descriptive statistics. We calculated the number of chemicals detected within the following chemical classes: polybrominated diphenyl ethers (PBDEs), perfluorinated compounds (PFCs), organochlorine pesticides, and phthalates and across multiple chemical classes. We compared chemical analyte concentrations for pregnant and nonpregnant women using least-squares geometric means, adjusting for demographic and physiological covariates.ResultsThe percentage of pregnant women with detectable levels of an individual chemical ranged from 0 to 100%. Certain polychlorinated biphenyls, organochlorine pesticides, PFCs, phenols, PBDEs, phthalates, polycyclic aromatic hydrocarbons, and perchlorate were detected in 99-100% of pregnant women. The median number of detected chemicals by chemical class ranged from 4 of 12 PFCs to 9 of 13 phthalates. Across chemical classes, median number ranged from 8 of 17 chemical analytes to 50 of 71 chemical analytes. We found, generally, that levels in pregnant women were similar to or lower than levels in nonpregnant women; adjustment for covariates tended to increase levels in pregnant women compared with nonpregnant women.ConclusionsPregnant women in the U.S. are exposed to multiple chemicals. Further efforts are warranted to understand sources of exposure and implications for policy making
Vaginal douching and racial/ethnic disparities in phthalates exposures among reproductive-aged women: National Health and Nutrition Examination Survey 2001–2004
Background
Diethyl phthalate (DEP) and di-n-butyl phthalate (DnBP) are industrial chemicals found in consumer products that may increase risk of adverse health effects. Although use of personal care/beauty products is known to contribute to phthalate exposure, no prior study has examined feminine hygiene products as a potential phthalate source. In this study, we evaluate whether vaginal douching and other feminine hygiene products increase exposure to phthalates among US reproductive-aged women. Methods
We conducted a cross-sectional study on 739 women (aged 20–49) from the National Health and Nutrition Examination Survey 2001–2004 to examine the association between self-reported use of feminine hygiene products (tampons, sanitary napkins, vaginal douches, feminine spray, feminine powder, and feminine wipes/towelettes) with urinary concentrations of monoethyl phthalate (MEP) and mono-n-butyl phthalate (MnBP), metabolites of DEP and DnBP, respectively. Results
A greater proportion of black women than white and Mexican American women reported use of vaginal douches, feminine spray, feminine powder, and wipes/towelettes in the past month whereas white women were more likely than other racial/ethnic groups to report use of tampons (p \u3c 0.05). Douching in the past month was associated with higher concentrations of MEP but not MnBP. No other feminine hygiene product was significantly associated with either MEP or MnBP. We observed a dose–response relationship between douching frequency and MEP concentrations (ptrend \u3c 0.0001); frequent users (≥2 times/month) had 152.2 % (95 % confidence intervals (CI): (68.2 %, 278.3 %)) higher MEP concentrations than non-users. We also examined whether vaginal douching mediates the relationship between race/ethnicity and phthalates exposures. Black women had 48.4 % (95 % CI: 16.8 %, 88.6 %; p = 0.0002) higher MEP levels than white women. Adjustment for douching attenuated this difference to 26.4 % (95 % CI:−0.9 %, 61.2 %; p = 0.06). Mediation effects of douching were statistically significant for black-white differences (z = 3.71, p \u3c 0.001) but not for differences between Mexican Americans and whites (z = 1.80, p = 0.07). Conclusions
Vaginal douching may increase exposure to DEP and contribute to racial/ethnic disparities in DEP exposure. The presence of environmental chemicals in vaginal douches warrants further examination
Reducing Chemical Exposures at Home: Opportunities For Action.
Indoor environments can influence human environmental chemical exposures and, ultimately, public health. Furniture, electronics, personal care and cleaning products, floor coverings and other consumer products contain chemicals that can end up in the indoor air and settled dust. Consumer product chemicals such as phthalates, phenols, flame retardants and per- and polyfluorinated alkyl substances are widely detected in the US general population, including vulnerable populations, and are associated with adverse health effects such as reproductive and endocrine toxicity. We discuss the implications of our recent meta-analysis describing the patterns of chemical exposures and the ubiquity of multiple chemicals in indoor environments. To reduce the likelihood of exposures to these toxic chemicals, we then discuss approaches for exposure mitigation: targeting individual behaviour change, household maintenance and purchasing decisions, consumer advocacy and corporate responsibility in consumer markets, and regulatory action via state/federal policies. There is a need to further develop evidence-based strategies for chemical exposure reduction in each of these areas, given the multi-factorial nature of the problem. Further identifying those at greatest risk; understanding the individual, household and community factors that influence indoor chemical exposures; and developing options for mitigation may substantially improve individuals’ exposures and health
Leukocyte Telomere Length in Relation to 17 Biomarkers of Cardiovascular Disease Risk: A Cross-Sectional Study of US Adults
Background
Leukocyte telomere length (LTL) is a putative biological marker of immune system age, and there are demonstrated associations between LTL and cardiovascular disease. This may be due in part to the relationship of LTL with other biomarkers associated with cardiovascular disease risk. However, the strength of associations between LTL and adiposity, metabolic, proinflammatory, and cardiovascular biomarkers has not been systematically evaluated in a United States nationally representative population. Methods and Findings
We examined associations between LTL and 17 cardiovascular biomarkers, including lipoproteins, blood sugar, circulatory pressure, proinflammatory markers, kidney function, and adiposity measures, in adults ages 20 to 84 from the cross-sectional US nationally representative 1999–2002 National Health and Nutrition Examination Survey (NHANES) (n = 7,252), statistically adjusting for immune cell type distributions. We also examine whether these associations differed systematically by age, race/ethnicity, gender, education, and income. We found that a one unit difference in the following biomarkers were associated with kilobase pair differences in LTL: BMI -0.00478 (95% CI -0.00749–-0.00206), waist circumference -0.00211 (95% CI -0.00325–-0.000969), percentage of body fat -0.00516 (95% CI -0.00761–-0.0027), high density lipoprotein (HDL) cholesterol 0.00179 (95% CI 0.000571–0.00301), triglycerides -0.000285 (95% CI -0.000555–-0.0000158), pulse rate -0.00194 (95% CI -0.00317–-0.000705), C-reactive protein -0.0363 (95% CI 0.0601–-0.0124), cystatin C -0.0391 (95% CI -0.0772–-0.00107). When using clinical cut-points we additionally found associations between LTL and insulin resistance -0.0412 (95% CI -0.0685–-0.0139), systolic blood pressure 0.0455 (95% CI 0.00137–0.0897), and diastolic blood pressure -0.0674 (95% CI -0.126–-0.00889). These associations were 10%–15% greater without controlling for leukocyte cell types. There were very few differences in the associations by age, race/ethnicity, gender, education, or income. Our findings are relevant to the relationships between these cardiovascular biomarkers in the general population but not to cardiovascular disease as a clinical outcome. Conclusions
LTL is most strongly associated with adiposity, but is also associated with biomarkers across several physiological systems. LTL may thus be a predictor of cardiovascular disease through its association with multiple risk factors that are physiologically correlated with risk for development of cardiovascular disease. Our results are consistent with LTL being a biomarker of cardiovascular aging through established physiological mechanisms
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