United States Environmental Protection Agency

About: United States Environmental Protection Agency is a government organization based out in Washington D.C., District of Columbia, United States. It is known for research contribution in the topics: Population & Environmental exposure. The organization has 13873 authors who have published 26902 publications receiving 1191729 citations. The organization is also known as: EPA & Environmental Protection Agency.

Halonitromethane drinking water disinfection byproducts: chemical characterization and mammalian cell cytotoxicity and genotoxicity.

Abstract: Halonitromethanes are drinking water disinfection byproducts that have recently received a high priority for health effects research from the U.S. Environmental Protection Agency (EPA). Our purpose was to identify and synthesize where necessary the mixed halonitromethanes and to determine the chronic cytotoxicity and the acute genotoxicity of these agents in mammalian cells. The halonitromethanes included bromonitromethane (BNM), dibromonitromethane (DBNM), tribromonitromethane (TBNM), bromochloronitromethane (BCNM), dibromochloronitromethane (DBCNM), bromodichloronitromethane (BDCNM), chloronitromethane (CNM), dichloronitromethane (DCNM), and trichloronitromethane (TCNM). Low- and high-resolution gas chromatography/mass spectrometry (GC/MS) was used to identify the mixed chloro-bromonitromethanes in finished drinking waters, and analytical standards that were not commercially available were synthesized (BDCNM, DBCNM, TBNM, CNM, DCNM, BCNM). The rank order of their chronic cytotoxicity (72 h exposure) to Chinese hamster ovary (CHO) cells was DBNM > DBCNM > BNM > TBNM > BDCNM > BCNM > DCNM > CNM > TCNM. The rank order to induce genomic DNA damage in CHO cells was DBNM > BDCNM > TBNM > TCNM > BNM > DBCNM > BCNM > DCNM > CNM. The brominated nitromethanes were more cytotoxic and genotoxic than their chlorinated analogues. This research demonstrated the integration of the procedures for the analytical chemistry and analytical biology when working with limited amounts of sample. The halonitromethanes are potent mammalian cell cytotoxins and genotoxins and may pose a hazard to the public health and the environment.

Inhibition of Testicular Steroidogenesis by the Xenoestrogen Bisphenol A Is Associated with Reduced Pituitary Luteinizing Hormone Secretion and Decreased Steroidogenic Enzyme Gene Expression in Rat Leydig Cells

Abstract: Exposure of humans to bisphenol A (BPA), a monomer in polycarbonate plastics and a constituent of resins used in food packaging and dentistry, is significant. In this report exposure of rats to 2.4 microg/kg.d (a dose that approximates BPA levels in the environment) from postnatal d 21-35 suppressed serum LH (0.21 +/- 0.05 ng/ml; vs. control, 0.52 +/- 0.04; P < 0.01) and testosterone (T) levels (1.62 +/- 0.16 ng/ml; vs. control, 2.52 +/- 0.21; P < 0.05), in association with decreased LHbeta and increased estrogen receptor beta pituitary mRNA levels as measured by RT-PCR. Treatment of adult Leydig cells with 0.01 nm BPA decreased T biosynthesis by 25% as a result of decreased expression of the steroidogenic enzyme 17alpha-hydroxylase/17-20 lyase. BPA decreased serum 17beta-estradiol levels from 0.31 +/- 0.02 ng/ml (control) to 0.22 +/- 0.02, 0.19 +/- 0.02, and 0.23 +/- 0.03 ng/ml in rats exposed to 2.4 microg, 10 microg, or 100 mg/kg.d BPA, respectively, from 21-35 d of age (P < 0.05) due to its ability to inhibit Leydig cell aromatase activity. Exposures of pregnant and nursing dams, i.e. from gestation d 12 to postnatal d 21, decreased T levels in the testicular interstitial fluid from 420 +/- 34 (control) to 261 +/- 22 (P < 0.05) ng/ml in adulthood, implying that the perinatal period is a sensitive window of exposure to BPA. As BPA has been measured in several human populations, further studies are warranted to assess the effects of BPA on male fertility.

Blood organic mercury and dietary mercury intake: National Health and Nutrition Examination Survey, 1999 and 2000.

Abstract: Blood organic mercury (i.e., methyl mercury) concentrations among 1,709 women who were participants in the National Health and Nutrition Examination Survey (NHANES) in 1999 and 2000 (1999-2000 NHANES) were 0.6 microg/L at the 50th percentile and ranged from concentrations that were nondetectable (5th percentile) to 6.7 microg/L (95th percentile). Blood organic/methyl mercury reflects methyl mercury intake from fish and shellfish as determined from a methyl mercury exposure parameter based on 24-hr dietary recall, 30-day food frequency, and mean concentrations of mercury in the fish/shellfish species reported as consumed (multiple correlation coefficient > 0.5). Blood organic/methyl mercury concentrations were lowest among Mexican Americans and highest among participants who designated themselves in the Other racial/ethnic category, which includes Asians, Native Americans, and Pacific Islanders. Blood organic/methyl mercury concentrations were ~1.5 times higher among women 30-49 years of age than among women 16-29 years of age. Blood mercury (BHg) concentrations were seven times higher among women who reported eating nine or more fish and/or shellfish meals within the past 30 days than among women who reported no fish and/or shellfish consumption in the past 30 days. Blood organic/methyl mercury concentrations greater than or equal to 5.8 microg/L were lowest among Mexican Americans (2.0%) and highest among examinees in the Other racial/ethnic category (21.7%). Based on the distribution of BHg concentrations among the adult female participants in 1999-2000 NHANES and the number of U.S. births in 2000, > 300,000 newborns each year in the United States may have been exposed in utero to methyl mercury concentrations higher than those considered to be without increased risk of adverse neurodevelopmental effects associated with methyl mercury exposure.

IPCS framework for analyzing the relevance of a noncancer mode of action for humans.

Abstract: Structured frameworks are extremely useful in promoting transparent, harmonized approaches to the risk assessment of chemicals. One area where this has been particularly successful is in the analysis of modes of action (MOAs) for chemical carcinogens in experimental animals and their relevance to humans. The International Programme on Chemical Safety (IPCS) recently published an updated version of its MOA framework in animals to address human relevance (cancer human relevance framework, or HRF). This work has now been extended to noncancer effects, with the eventual objective of harmonizing framework approaches to both cancer and noncancer endpoints. As in the cancer HRF, the first step is to determine whether the weight of evidence based on experimental observations is sufficient to establish a hypothesized MOA. This comprises a series of key events causally related to the toxic effect, identified using an approach based on the Bradford Hill criteria. These events are then compared qualitatively and, next, quantitatively between experimental animals and humans. The output of the analysis is a clear statement of conclusions, together with the confidence, analysis, and implications of the findings. This framework provides a means of ensuring a transparent evaluation of the data, identification of key data gaps and of information that would be of value in the further risk assessment of the compound, such as on dose-response relationships, and recognition of potentially susceptible subgroups, for example, based on life-stage considerations.