Mary Jane K. Selgrade
United States Environmental Protection Agency
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Environmental Health Perspectives | 2006
Mary Jane K. Selgrade; Robert F. Lemanske; M. Ian Gilmour; Lucas M. Neas; Marsha D. W. Ward; Paul K. Henneberger; David N. Weissman; Jane A. Hoppin; Rodney R. Dietert; Peter D. Sly; Andrew M. Geller; Paul L. Enright; Gillian S. Backus; Philip A. Bromberg; Dori R. Germolec; Karin Yeatts
The prevalence of asthma has increased dramatically over the last 25 years in the United States and in other nations as a result of ill-defined changes in living conditions in modern society. On 18 and 19 October 2004 the U.S. Environmental Protection Agency and the National Institute of Environmental Health Sciences sponsored the workshop “Environmental Influences on the Induction and Incidence of Asthma” to review current scientific evidence with respect to factors that may contribute to the induction of asthma. Participants addressed two broad questions: a) What does the science suggest that regulatory and public health agencies could do now to reduce the incidence of asthma? and b) What research is needed to improve our understanding of the factors that contribute to the induction of asthma and our ability to manage this problem? In this article (one of four articles resulting from the workshop), we briefly characterize asthma and its public health and economic impacts, and intervention strategies that have been successfully used to prevent induction of asthma in the workplace. We conclude with the findings of seven working groups that focus on ambient air, indoor pollutants (biologics), occupational exposures, early life stages, older adults, intrinsic susceptibility, and lifestyle. These groups found strong scientific support for public health efforts to limit in utero and postnatal exposure to cigarette smoke. However, with respect to other potential types of interventions, participants noted many scientific questions, which are summarized in this article. Research to address these questions could have a significant public health and economic impact that would be well worth the investment.
Toxicology | 2000
Marsha D. W. Ward; Sharon L. Madison; Debora L. Andrews; Denise M. Sailstad; Stephen H. Gavett; Mary Jane K. Selgrade
Metarhizium anisopliae, an entomopathogenic fungus, is a prototypic microbial pesticide licensed for indoor control of cockroaches, a major source of allergens. We have previously demonstrated allergy and asthma-like responses in BALB/c mice intraperitoneally (IP) sensitized in the presence of adjuvant and intratracheally (IT) challenged with the soluble factors from M. anisopliae crude antigen (MACA) (Ward et al., 1998, 2000). This protocol has been used frequently to establish animal models of allergenicity. However, the sensitization protocol is artificial and not representative of an environmental exposure. Concern has been raised that this protocol might produce allergic responses that would not occur under normal environmental exposure conditions. The objective of this study was to compare responses in mice to MACA by two exposure protocols: (1) exclusive respiratory exposures without adjuvant (representative of environmental exposures) and (2) intraperitoneal sensitization in the presence of adjuvant followed by IT challenge (the traditional approach). The intratracheal protocol consisted of four IT exposures of 10 microg MACA in 50 microl HBSS each over a 4-week period. A vehicle control group of mice was exposed IT to HBSS. The intraperitoneal protocol consisted of IP sensitization with 25 microg MACA in 0.2 ml of 1.3% alhydrogel (aluminum hydroxide) followed 14 days later with an IT challenge (10 microg MACA/50 microl HBSS). Airway reactivity responsiveness to methacholine was assessed, serum and bronchoalveolar lavage fluid (BALF) samples were obtained, and the lungs were fixed for histopathology at 1, 3, and 8 days following the last MACA IT challenge. Both groups exhibited immune and pulmonary responses typical of allergic asthma. In general, local responses in the lung, including inflammatory responses (eosinophils, lymphocytes, and macrophages), BALF IgE, and functional responses to methacholine were greater in the IT sensitized group compared to the IP sensitized group, whereas the systemic IgE response was greater in the IP sensitized group. The BALF IL-5 cytokine levels were elevated before and throughout the eosinophil influx. IL-4 was detected in the BALF of IP sensitized, but not IT sensitized mice. Histopathologic changes in the two groups were similar in nature but more severe in the IT mice. The results suggest that the IP sensitization protocol does not induce the level of respiratory responsiveness that results from sensitization by a physiologically relevant route of exposure. Thus total serum IgE levels, which were greater following IP sensitization, may not be the best indicator of allergen potency, at least with respect to respiratory responses.
International Journal of Immunopharmacology | 1988
Mary Jane K. Selgrade; Mary J. Daniels; Gary R. Burleson; Lloyd D. Lauer; Jack H. Dean
Susceptibility to murine cytomegalovirus (MCMV) was enhanced by treating B6C3F1 and CD-1 mice subcutaneously with 100 mg 7,12-dimethyl-benz[a]anthracene (DMBA)/kg fractionated over a 2 week period prior to sub-lethal infection. Virus-augmented natural killer cell (NKC) activity was depressed in B6C3F1 mice treated with 100 mg DMBA/kg, while serum interferon (IFN) levels were unaffected. Treatment with 50 mg DMBA/kg had no effect on susceptibility to virus or virus-augmented NKC activity. Susceptibility to MCMV was not affected by treating mice with 400 mg benzo[a]pyrene (B[a]P)/kg using the same exposure regimen. Virus-augmented NKC activity was suppressed in B[a]P-treated mice, but the magnitude of the suppression (18%) was much less than that for DMBA-treated mice (39%). Susceptibility to MCMV, virus-augmented NKC and IFN induction were not affected in mice treated intraperitoneally with 50 mg cyclosporin A (CSA)/kg/day for 5 days and infected on the 5th day of treatment. In contrast, enhanced susceptibility to MCMV and depressed NKC activity were observed in mice treated by the same exposure regimen on days 1-5 post infection. Susceptibility was not affected by CSA given on days 5-9 post infection. The data are useful not only because they show that DMBA and appropriately-timed CSA treatments suppress virus augmented NKC and enhance susceptibility to MCMV, but also because they help to define the relative importance of certain immune responses in defending against the infection, thus improving the usefulness of MCMV as a host resistance model for immunotoxicity testing. The data suggest that chemicals which depress NKC are likely to enhance susceptibility to MCMV, and conversely that effects on NKC should be suspected when chemical exposure enhances susceptibility to MCMV.
Toxicological Sciences | 2010
Robert V. House; Mary Jane K. Selgrade
The Immunotoxicology Specialty Section of the Society of Toxicology celebrated its 25th anniversary at the 2010 Annual Meeting, prompting us to provide here both an historical perspective and an assessment of the challenges that lie ahead for this subdiscipline of toxicology. In 1985, immunotoxicology focused primarily on use of rodent models to evaluate suppression of adaptive immune responses (which our peers sometimes considered obscure), as well as evaluation of allergic responses to chemicals, primarily allergic contact dermatitis. Apart from a common organ system, immune suppression and allergy were considered totally separate disciplines. Innate and adaptive immunity were also viewed as independent entities, and at the time, the adaptive immune system received more attention from immunotoxicologists because it was the hot area in immunology. Innate immunity was perceived as evolutionarily ‘‘ancient’’ and therefore less relevant. What a difference a few decades makes. Twenty-five years ago because AIDS had only recently been identified, both the scientific community and the public at large were acutely aware of the adverse results of immune suppression and the important role that T lymphocytes play in maintaining good health. (As a result, there was substantial funding for basic T-cell immunology.) Hence, these were de facto the hot topic for immunotoxicology. Polychlorinated biphenyls were the first class of chemicals studies followed shortly thereafter by halogenated hydrocarbons (dioxin and others), heavy metals, and some organotins (Moore, 1979). In the beginning, testing for immune suppression relied primarily on routine histopathology and research to develop better tests focused on host resistance models and functional assays in laboratory rodents (Vos, 1977). Compatibility between rodent tests and human studies was nonexistent. Through much effort and interlaboratory collaboration the concept of ‘‘tier testing’’ was developed, the springboard for much of immunotoxicology for the 90s (Luster et al., 1988). Meanwhile, tests for hypersensitivity relied mostly on skin painting guinea pigs and humans and observing dermal erythema and edema (Botham et al., 1991); other types of allergic and autoimmune responses were largely untouched. Risk assessors wondered what to make of our discipline. Twenty-five years later, we are thinking much more in terms of modulation of the immune system rather than immune suppression, hypersensitivity, or autoimmunity as isolated entities. Certain immune function tests have been included in harmonized test guidelines (U.S. Environmental Protection Agency, 1998, 2003; ICHS8, 2006; OECD, 1995), and specific examples of immune suppression in the human population have been found that mirror results seen in laboratory animals (Luebke et al., 2004; Selgrade, 2007). Our understanding of how to interpret results of these tests in risk assessment has vastly improved (Germolec, 2004), although consensus has yet to be reached. Guinea pig tests have given way to the more mechanistically based local lymph node assay for predicting the likelihood that an exposure will result in allergic contact dermatitis (Gerberick et al., 2007), opening the door for more quantitative risk assessment (Griem et al., 2003). Even autoimmunity—long one of the most difficult forms of immunotoxicity to understand—is coming into better focus (Dietert et al., 2010). Much has been accomplished, but much remains to be done, and the field is open for the next generation(s) of immunotoxicologists to make further advancements in the following areas:
Toxicological Sciences | 1994
Denise M. Sailstad; Jeffrey S. Tepper; Donald L. Doerfler; Mohammad Qasim; Mary Jane K. Selgrade
Two dye mixtures and the individual component dyes were evaluated for the potential to induce contact or pulmonary hypersensitivity. These dye mixtures were suspect because of anecdotal reports of both pulmonary and contact hypersensitivity in assembly workers, and because the component dyes were structurally related to dyes known to be contact sensitizers. One mixture consisted of disperse blue 3 (DB3) and disperse red 11 (DR11), which are anthraquinones, and the other mixture contained DR11 and solvent red 1 (SR1), an azo dye. Contact hypersensitivity was examined using the local lymph node assay (LLNA) and a modified mouse ear swelling test (MEST). Both the MEST and the LLNA indicated that SR1 has weak contact-sensitizing potential. None of the other individual dye compounds or the two mixtures were identified as contact sensitizers by either method. To evaluate the mixtures as potential pulmonary allergens, guinea pigs were repeatedly exposed by inhalation (300 mg/m3, 6 hr/day) 5 days/week, for 1 week. Weekly exposures were repeated three times with 2 weeks of nonexposure time in between. Guinea pigs were then challenged through the jugular vein using a dye-dimethylsulfoxide mixture. During the challenge, breathing mechanics (dynamic compliance and resistance) were measured in mechanically ventilated animals. Changes in these measurements, indicative of bronchoconstriction, were not observed in animals exposed to either dye mixture, nor were antibodies detected in the sera of exposed animals using individual dye-specific enzyme-linked immunosorbent assays. In conclusion, two methods indicate that SR1 may have contact-sensitizing potential.(ABSTRACT TRUNCATED AT 250 WORDS)
Archive | 2018
Cynthia V. Rider; Thais C. Morata; Mary Jane K. Selgrade; Kenneth G. Sexton
Physical stressors represent an important class of factors that can affect the health of humans or ecosystems and should be considered in cumulative risk assessment. Physical stressors are defined here as biological agents (e.g., bacteria, viruses) or external forces (e.g., radiation, noise) that can modify exposure and/or elicit a physiological response from the exposed organism. Physical stressors can intersect with chemical stressors in at least three ways: (1) by directly interacting with chemicals to modify exposure (e.g., photoreactions of sunlight with air pollution), (2) by interacting with the same target system as a chemical stressor to elicit joint effects (e.g., noise and chemicals can both affect the physiological mechanism leading to hearing disorders), and (3) by interacting with the target system to alter its susceptibility or response to chemical exposure (e.g., virus-initiated disease leading to hyper-responsiveness to chemical insult). In this chapter, physical stressors will be discussed in terms of their actions on biological systems, modification of exposure or effects of chemical stressors, and suggestions for incorporation into cumulative risk assessment.
Toxicological Sciences | 2006
Michael P. Holsapple; David Jones; Thomas T. Kawabata; Ian Kimber; Kathy Sarlo; Mary Jane K. Selgrade; Jui Shah; Michael R. Woolhiser
Photochemistry and Photobiology | 2000
Lisa K. Ryan; Donna L. Neldon; Lisa R. Bishop; M. Ian Gilmour; Mary J. Daniels; Denise M. Sailstad; Mary Jane K. Selgrade
Regulatory Toxicology and Pharmacology | 2016
Colin M. North; Janine Ezendam; Jon A. Hotchkiss; Curtis Maier; Kohji Aoyama; Steve Enoch; Amber K. Goetz; Cynthia Graham; Ian Kimber; Antti Karjalainen; Juergen Pauluhn; Erwin Ludo Roggen; Mary Jane K. Selgrade; Susan M. Tarlo; Connie L. Chen
Toxicological Sciences | 2014
Cynthia V. Rider; Kim Boekelheide; Natasha Catlin; Christopher J. Gordon; Thais C. Morata; Mary Jane K. Selgrade; Kenneth G. Sexton; Jane Ellen Simmons