Interaction between gas cooking and<i>GSTM1</i>null genotype in bronchial responsiveness: results from the European Community Respiratory Health Survey

Amaral, André F.S.; Ramasamy, Adaikalavan; Castro-Giner, Francesc; Minelli, Cosetta; Accordini, Simone; Sorheim, I.-C.; Pin, Isabelle; Kogevinas, Manolis; Jõgi, Rain; Balding, David J.; Norbäck, Dan; Verlato, G.; Olivieri, Mario; Probst‐Hensch, Nicole; Janson, Christer; Zock, Jan‐Paul; Heinrich, Joachim; Jarvis, Déborah

doi:10.1136/thoraxjnl-2013-204574

Cited by 21 publications

(11 citation statements)

References 32 publications

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“…Gene-environment interactions between the IL-4 promoter and an indoor mold may play an important role in childhood asthma (82). Increased BHR in adults was associated with gas cooking (a major indoor source of NO2), but only among subjects with the GSTM1 null genotype (83). IL-13 variants were found to interact with household carpet use on the risk of asthma in Taiwanese children (84).…”

Section: Indoor Exposuresmentioning

confidence: 99%

Genetics and Gene-Environment Interactions in Childhood and Adult Onset Asthma

Morales

Duffy

2019

Front. Pediatr.

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Asthma is a heterogeneous disease that results from the complex interaction between genetic factors and environmental exposures that occur at critical periods throughout life. It seems plausible to regard childhood-onset and adult-onset asthma as different entities, each with a different pathophysiology, trajectory, and outcome. This review provides an overview about the role of genetics and gene-environment interactions in these two conditions. Looking at the genetic overlap between childhood and adult onset disease gives one window into whether there is a correlation, as well as to mechanism. A second window is offered by the genetics of the relationship between each type of asthma and other phenotypes e.g., obesity, chronic obstructive pulmonary disease (COPD), atopy, vitamin D levels, and inflammatory and immune status; and third, the genetic-specific responses to the many environmental exposures that influence risk throughout life, and particularly those that occur during early-life development. These represent a large number of possible combinations of genetic and environmental factors, at least 150 known genetic loci vs. tobacco smoke, outdoor air pollutants, indoor exposures, farming environment, and microbial exposures. Considering time of asthma onset extends the two-dimensional problem of gene-environment interactions to a three-dimensional problem, since identified gene-environment interactions seldom replicate for childhood and adult asthma, which suggests that asthma susceptibility to environmental exposures may biologically differ from early life to adulthood as a result of different pathways and mechanisms of the disease.

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Section: Indoor Exposuresmentioning

confidence: 99%

Genetics and Gene-Environment Interactions in Childhood and Adult Onset Asthma

Morales

Duffy

2019

Front. Pediatr.

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“…In addition to lower levels of superoxide dismutase and catalase, 89 it has been shown that goblet cells express the high-affinity sodium ascorbate cotransporter, which is involved in vitamin C uptake into cells, and that expression of sodium ascorbate cotransporters is inversely related to lung lining fluid vitamin C levels 91 . There is also considerable evidence that polymorphisms in glutathione -cycling enzymes can result in increased susceptibility to air pollution 92, 93, 94. Glutathione-S-transferase (GST)-pi is predominantly expressed in airway epithelial cells, and expression is decreased in the airways of children with asthma 95 .…”

Section: Dysregulation Of the Epithelial Barrier In Asthmatic Patientsmentioning

confidence: 99%

Phenotypic and genetic aspects of epithelial barrier function in asthmatic patients

Loxham

Davies

2017

Journal of Allergy and Clinical Immunology

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The bronchial epithelium is continuously exposed to a multitude of noxious challenges in inhaled air. Cellular contact with most damaging agents is reduced by the action of the mucociliary apparatus and by formation of a physical barrier that controls passage of ions and macromolecules. In conjunction with these defensive barrier functions, immunomodulatory cross-talk between the bronchial epithelium and tissue-resident immune cells controls the tissue microenvironment and barrier homeostasis. This is achieved by expression of an array of sensors that detect a wide variety of viral, bacterial, and nonmicrobial (toxins and irritants) agents, resulting in production of many different soluble and cell-surface molecules that signal to cells of the immune system. The ability of the bronchial epithelium to control the balance of inhibitory and activating signals is essential for orchestrating appropriate inflammatory and immune responses and for temporally modulating these responses to limit tissue injury and control the resolution of inflammation during tissue repair. In asthmatic patients abnormalities in many aspects of epithelial barrier function have been identified. We postulate that such abnormalities play a causal role in immune dysregulation in the airways by translating gene-environment interactions that underpin disease pathogenesis and exacerbation.

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“…On the same topic we were delighted to publish a systematic review35 of the adverse effects of PM 2.5 pollution (‘it's bad for you’)—a gargantuan effort and a thoroughly ‘worthy’ paper. Nor did we ignore the indoor; in June we published a manuscript on the risks of cooking with gas 36. No overall effect on bronchial responsiveness was found, but those with a null GSTM1 genotype were more responsive if they cooked with gas, especially if they use bottled gas or a stove with both a gas hob and an oven or if their kitchen was unventilated.…”

Section: Epidemiologymentioning

confidence: 99%