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The effects of environmental toxins on allergic inflammation.

Yang SN, Hsieh CC, Kuo HF, Lee MS, Huang MY, Kuo CH, Hung CH - Allergy Asthma Immunol Res (2014)

Bottom Line: Many common environmental factors are associated with this increase.These data are consistent with epidemiological research that has consistently detected increased incidences of allergies and asthma in people living in these locations.During recent decades more than 100,000 new chemicals have been used in common consumer products and are released into the everyday environment.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, E-DA Hospital, Kaohsiung, Taiwan. ; School of Medicine, College of Medicine, I-Shou University, Kaohsiung, Taiwan.

ABSTRACT
The prevalence of asthma and allergic disease has increased worldwide over the last few decades. Many common environmental factors are associated with this increase. Several theories have been proposed to account for this trend, especially those concerning the impact of environmental toxicants. The development of the immune system, particularly in the prenatal period, has far-reaching consequences for health during early childhood, and throughout adult life. One underlying mechanism for the increased levels of allergic responses, secondary to exposure, appears to be an imbalance in the T-helper function caused by exposure to the toxicants. Exposure to environmental endocrine-disrupting chemicals can result in dramatic changes in cytokine production, the activity of the immune system, the overall Th1 and Th2 balance, and in mediators of type 1 hypersensitivity mediators, such as IgE. Passive exposure to tobacco smoke is a common risk factor for wheezing and asthma in children. People living in urban areas and close to roads with a high volume of traffic, and high levels of diesel exhaust fumes, have the highest exposure to environmental compounds, and these people are strongly linked with type 1 hypersensitivity disorders and enhanced Th2 responses. These data are consistent with epidemiological research that has consistently detected increased incidences of allergies and asthma in people living in these locations. During recent decades more than 100,000 new chemicals have been used in common consumer products and are released into the everyday environment. Therefore, in this review, we discuss the environmental effects on allergies of indoor and outside exposure.

No MeSH data available.


Related in: MedlinePlus

Possible mechanisms of the effects of environmental toxins on allergic inflammation. Alkyphenols and phthalates alter the function of human plasmacytoid dendritic cells (pDC) and myeloid DCs (mDC) by changing the expression cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-10, interferon (IFN)-α and IFN-β via the epigenetic regulation by histone acetylation as well as trimethylation. Alkyphenols and phthalates change the T cell stimulation function of DCs that promote Th2 development but suppress Th1 development. Heavy metals suppress Th1 development by inhibiting IFN-γ expression and promote Th2 development by enhancing IL-4 expression, and increase the production of IgE. Heavy metals also increase IgE-dependent basophil-mediated inflammation. Tobacco smoke suppresses the Th1 immune response by inhibiting IFN-γ expression and the survival of natural killer T cells, and promotes the Th2 immune response by increasing IL-4, IL-5, and IL-13 expression. Diesel exhaust particles increase IgE levels, and pulmonary and systemic Th2 and Th17 cytokine levels.
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Figure 1: Possible mechanisms of the effects of environmental toxins on allergic inflammation. Alkyphenols and phthalates alter the function of human plasmacytoid dendritic cells (pDC) and myeloid DCs (mDC) by changing the expression cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-10, interferon (IFN)-α and IFN-β via the epigenetic regulation by histone acetylation as well as trimethylation. Alkyphenols and phthalates change the T cell stimulation function of DCs that promote Th2 development but suppress Th1 development. Heavy metals suppress Th1 development by inhibiting IFN-γ expression and promote Th2 development by enhancing IL-4 expression, and increase the production of IgE. Heavy metals also increase IgE-dependent basophil-mediated inflammation. Tobacco smoke suppresses the Th1 immune response by inhibiting IFN-γ expression and the survival of natural killer T cells, and promotes the Th2 immune response by increasing IL-4, IL-5, and IL-13 expression. Diesel exhaust particles increase IgE levels, and pulmonary and systemic Th2 and Th17 cytokine levels.

Mentions: Pesticides are widely used to control pest and pest-related diseases in agriculture, fishery, forestry, and also in the food industry. There are a number of respiratory diseases and symptoms that have been associated with occupational exposure to pesticides. Impaired lung function has also been found in people suffering from allergies who are occupationally exposed to pesticides. Several respiratory symptoms, such as coughing, wheezing and airway inflammation, are commonly observed in people exposed to pesticides.55,56 Exposure to pesticides in utero has been reported as a risk for childhood asthma.57 There is strong evidence of an association between occupational exposure to pesticides and asthma, especially in agriculture. If the fetus is exposed to certain pesticides during pregnancy, allergies and hay fever appear to be more common in the offspring, and especially in the male offspring.57 The potential effects of early exposure to pesticides may be confounded by the generally protective effects of in utero exposure to the farmyard environment and exposure to livestock. Livestock farmers on farms had significantly lower incidences of allergic rhinitis than crop farmers.58 There is little antigenicity in chemical pesticides, pesticide-induced or -promoted allergic/atopic asthma. Therefore, pesticide-induced allergy may be due to the indirect effects of pesticides on the immune system, such as interfering with the Th1/Th2 balance, or pesticide-induced oxidative stress.59 There is an urgent need for training and education on basic safety precautions and the proper use of personal protection equipment. This type of intervention could control the incidences of respiratory disease associated with pesticide exposure in an occupational setting. We summary the potential immunological mechanisms induced by environmental toxicant on allergic inflammation in Table and Figure.


The effects of environmental toxins on allergic inflammation.

Yang SN, Hsieh CC, Kuo HF, Lee MS, Huang MY, Kuo CH, Hung CH - Allergy Asthma Immunol Res (2014)

Possible mechanisms of the effects of environmental toxins on allergic inflammation. Alkyphenols and phthalates alter the function of human plasmacytoid dendritic cells (pDC) and myeloid DCs (mDC) by changing the expression cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-10, interferon (IFN)-α and IFN-β via the epigenetic regulation by histone acetylation as well as trimethylation. Alkyphenols and phthalates change the T cell stimulation function of DCs that promote Th2 development but suppress Th1 development. Heavy metals suppress Th1 development by inhibiting IFN-γ expression and promote Th2 development by enhancing IL-4 expression, and increase the production of IgE. Heavy metals also increase IgE-dependent basophil-mediated inflammation. Tobacco smoke suppresses the Th1 immune response by inhibiting IFN-γ expression and the survival of natural killer T cells, and promotes the Th2 immune response by increasing IL-4, IL-5, and IL-13 expression. Diesel exhaust particles increase IgE levels, and pulmonary and systemic Th2 and Th17 cytokine levels.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4214967&req=5

Figure 1: Possible mechanisms of the effects of environmental toxins on allergic inflammation. Alkyphenols and phthalates alter the function of human plasmacytoid dendritic cells (pDC) and myeloid DCs (mDC) by changing the expression cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-10, interferon (IFN)-α and IFN-β via the epigenetic regulation by histone acetylation as well as trimethylation. Alkyphenols and phthalates change the T cell stimulation function of DCs that promote Th2 development but suppress Th1 development. Heavy metals suppress Th1 development by inhibiting IFN-γ expression and promote Th2 development by enhancing IL-4 expression, and increase the production of IgE. Heavy metals also increase IgE-dependent basophil-mediated inflammation. Tobacco smoke suppresses the Th1 immune response by inhibiting IFN-γ expression and the survival of natural killer T cells, and promotes the Th2 immune response by increasing IL-4, IL-5, and IL-13 expression. Diesel exhaust particles increase IgE levels, and pulmonary and systemic Th2 and Th17 cytokine levels.
Mentions: Pesticides are widely used to control pest and pest-related diseases in agriculture, fishery, forestry, and also in the food industry. There are a number of respiratory diseases and symptoms that have been associated with occupational exposure to pesticides. Impaired lung function has also been found in people suffering from allergies who are occupationally exposed to pesticides. Several respiratory symptoms, such as coughing, wheezing and airway inflammation, are commonly observed in people exposed to pesticides.55,56 Exposure to pesticides in utero has been reported as a risk for childhood asthma.57 There is strong evidence of an association between occupational exposure to pesticides and asthma, especially in agriculture. If the fetus is exposed to certain pesticides during pregnancy, allergies and hay fever appear to be more common in the offspring, and especially in the male offspring.57 The potential effects of early exposure to pesticides may be confounded by the generally protective effects of in utero exposure to the farmyard environment and exposure to livestock. Livestock farmers on farms had significantly lower incidences of allergic rhinitis than crop farmers.58 There is little antigenicity in chemical pesticides, pesticide-induced or -promoted allergic/atopic asthma. Therefore, pesticide-induced allergy may be due to the indirect effects of pesticides on the immune system, such as interfering with the Th1/Th2 balance, or pesticide-induced oxidative stress.59 There is an urgent need for training and education on basic safety precautions and the proper use of personal protection equipment. This type of intervention could control the incidences of respiratory disease associated with pesticide exposure in an occupational setting. We summary the potential immunological mechanisms induced by environmental toxicant on allergic inflammation in Table and Figure.

Bottom Line: Many common environmental factors are associated with this increase.These data are consistent with epidemiological research that has consistently detected increased incidences of allergies and asthma in people living in these locations.During recent decades more than 100,000 new chemicals have been used in common consumer products and are released into the everyday environment.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, E-DA Hospital, Kaohsiung, Taiwan. ; School of Medicine, College of Medicine, I-Shou University, Kaohsiung, Taiwan.

ABSTRACT
The prevalence of asthma and allergic disease has increased worldwide over the last few decades. Many common environmental factors are associated with this increase. Several theories have been proposed to account for this trend, especially those concerning the impact of environmental toxicants. The development of the immune system, particularly in the prenatal period, has far-reaching consequences for health during early childhood, and throughout adult life. One underlying mechanism for the increased levels of allergic responses, secondary to exposure, appears to be an imbalance in the T-helper function caused by exposure to the toxicants. Exposure to environmental endocrine-disrupting chemicals can result in dramatic changes in cytokine production, the activity of the immune system, the overall Th1 and Th2 balance, and in mediators of type 1 hypersensitivity mediators, such as IgE. Passive exposure to tobacco smoke is a common risk factor for wheezing and asthma in children. People living in urban areas and close to roads with a high volume of traffic, and high levels of diesel exhaust fumes, have the highest exposure to environmental compounds, and these people are strongly linked with type 1 hypersensitivity disorders and enhanced Th2 responses. These data are consistent with epidemiological research that has consistently detected increased incidences of allergies and asthma in people living in these locations. During recent decades more than 100,000 new chemicals have been used in common consumer products and are released into the everyday environment. Therefore, in this review, we discuss the environmental effects on allergies of indoor and outside exposure.

No MeSH data available.


Related in: MedlinePlus