Publications by authors named "Kathleen Attfield"

E-cigarettes are battery-operated devices that heat a liquid mixture to make an aerosol that is inhaled, or vaped, by the user. Vape shops are retail environments designed to fulfill customer demand for diverse e-liquid flavors and hardware options, which create unique worker exposure concerns. To characterize exposures to vape shop workers, especially to flavoring chemicals associated with known respiratory toxicity, this study recruited vape shops from the San Francisco Bay Area.

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E-cigarettes utilize a wide range of flavoring chemicals with respiratory health effects that are not well understood. In this study, we used pulmonary-associated cell lines to assess the in vitro cytotoxic effects of 30 flavoring chemicals. Human bronchial epithelial cells (BEAS-2B) and both naïve and activated macrophages (THP-1) were treated with 10, 100, and 1000 µM of flavoring chemicals and analyzed for changes in viability, cell membrane damage, reactive oxygen species (ROS) production, and inflammatory cytokine release.

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Importance: Since August 2019, more than 2700 patients have been hospitalized with e-cigarette, or vaping, product use-associated lung injury (EVALI) across the United States. This report describes the outbreak in California, a state with one of the highest case counts and with a legal adult-use (recreational) cannabis market.

Objective: To present clinical characteristics and vaping product exposures of patients with EVALI in California.

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Background: Age at female puberty is associated with adult morbidities, including breast cancer and diabetes. Hormonally active chemicals are suspected of altering pubertal timing. We examined whether persistent organic pollutants (POPs) are associated with age at menarche in a longitudinal study.

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The use of electronic nicotine delivery systems continues to gain popularity, and there is concern for potential health risks from inhalation of aerosol and vapor produced by these devices. An analytical method was developed that provided quantitative and qualitative chemical information for characterizing the volatile constituents of bulk electronic cigarette liquids (e-liquids) using a static headspace technique. Volatile organic compounds (VOCs) were screened from a convenience sample of 146 e-liquids by equilibrating 1 g of each e-liquid in amber vials for 24 h at room temperature.

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Persons who died of Ebola virus disease at home in rural communities in Liberia and Guinea resulted in more secondary infections than persons admitted to Ebola treatment units. Intensified monitoring of contacts of persons who died of this disease in the community is an evidence-based approach to reduce virus transmission in rural communities.

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We measured the reproduction number before and after interventions were implemented to reduce Ebola transmission in 9 outbreaks in Liberia during 2014. We evaluated risk factors for secondary cases and the association between patient admission to an Ebola treatment unit (ETU) and survival. The reproduction number declined 94% from 1.

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West Africa is experiencing its first epidemic of Ebola virus disease (Ebola). As of February 9, Liberia has reported 8,864 Ebola cases, of which 3,147 were laboratory-confirmed. Beginning in August 2014, the Liberia Ministry of Health and Social Welfare (MOHSW), supported by CDC, the World Health Organization (WHO), and others, began systematically investigating and responding to Ebola outbreaks in remote areas.

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Background: Exposure to chemicals that cause rodent mammary gland tumors is common, but few studies have evaluated potential breast cancer risks of these chemicals in humans.

Objective: The goal of this review was to identify and bring together the needed tools to facilitate the measurement of biomarkers of exposure to potential breast carcinogens in breast cancer studies and biomonitoring.

Methods: We conducted a structured literature search to identify measurement methods for exposure biomarkers for 102 chemicals that cause rodent mammary tumors.

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Background: Children are exposed to pesticides from many sources and routes, including dietary and incidental ingestion, dermal absorption, and inhalation. Linking health outcomes to these exposures using urinary metabolites requires understanding temporal variability within subjects to avoid exposure misclassification.

Objectives: We characterized the within- and between-child variability of urinary organophosphorus and pyrethroid metabolites in 23 participants of the Children's Pesticide Exposure Study-Washington over 1 year and examined the ability of one to four spot urine samples to categorize mean exposures.

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We designed this community-based participatory research (CBPR) project aiming to generate evidence-based research results to encourage residents living in urban low-income public housing dwellings engaging in a community-wide integrated pest management (IPM) program with the intention to improve their health and quality of life, as well as household conditions. We enrolled 20 families and their children in this study in which we utilized environmental exposure assessment (surface wipe and indoor air) tools to quantitatively assessing residential pesticide exposure in young children before the implementation of an IPM program. We analyzed those samples for 19 organophosphate (OP) and pyrethroid pesticides.

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Increasing residential development in watershed recharge areas increases the likelihood of groundwater and surface water contamination by wastewater effluent, particularly where on-site sewage treatment is employed. This effluent contains a range of compounds including those that have been demonstrated to mimic or interfere with the function of natural hormones in aquatic organisms and humans. To explore whether groundwater contaminated by discharge from on-site septic systems affects water quality in surface water ecosystems, we measured steroidal hormones, pharmaceuticals, and other organic wastewater compounds (OWCs) in water collected from six aquifer-fed ponds in areas of higher and lower residential density on Cape Cod (Massachusetts, USA).

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Breast cancer is the most common invasive cancer in women worldwide and the leading cause of death in US women in mid-life. Treatment has adverse effects, adding to the importance of finding modifiable risk factors. At the invitation of Susan G.

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Laboratory research has shown that numerous environmental pollutants cause mammary gland tumors in animals; are hormonally active, specifically mimicking estrogen, which is a breast cancer risk factor; or affect susceptibility of the mammary gland to carcinogenesis. An assessment of epidemiologic research on these pollutants identified in toxicologic studies can guide future research and exposure reduction aimed at prevention. The PubMed database was searched for relevant literature and systematic critical reviews were entered in a database available at URL: www.

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Identifying chemical carcinogens in animal studies is currently the primary means of anticipating cancer effects in humans. Animal studies to evaluate potential chemical carcinogenicity are particularly important for breast cancer because environmental and occupational epidemiologic research is sparse. Chemicals that increased mammary gland tumors in animal studies were compiled from the International Agency for Research on Cancer (IARC), the U.

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XGef was isolated in a screen for proteins interacting with CPEB, a regulator of mRNA translation in early Xenopus development. XGef is a Rho-family guanine nucleotide exchange factor and activates Cdc42 in mammalian cells. Endogenous XGef (58 kDa) interacts with recombinant CPEB, and recombinant XGef interacts with endogenous CPEB in Xenopus oocytes.

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The ATP(CTP):tRNA nucleotidyltransferase (CCA-adding enzyme) adds CCA to the 3(') end of immature or damaged tRNAs. It is reported on here the cloning, expression analysis, and functional characterization of the Xenopus CCA-adding enzyme, XCCA (GenBank Accession #AF466151). It is demonstrated that XCCA adds cytosine and adenosine residues to the ends of prepared tRNA and is therefore a functional CCA-adding enzyme.

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