1045d2b8-9fed-4874-9117-1e569f05d480.json

{
 "id": "1045d2b8-9fed-4874-9117-1e569f05d480",
 "disease": {
  "id": "H00079",
  "names": [
   "Asthma"
  ],
  "dbLinks": {
   "icd10": [
    "J45"
   ],
   "mesh": [
    "D001249"
   ]
  },
  "category": "Immune system disease",
  "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation."
 },
 "article": {
  "id": "28926373",
  "text": "BACKGROUND:\nEarly-life exposure to traffic-related air pollution exacerbates childhood asthma, but it is unclear what role it plays in asthma development.\n\nMETHODS:\nThe association between exposure to primary mobile source pollutants during pregnancy and during infancy and asthma incidence by ages 2 through 6 was examined in the Kaiser Air Pollution and Pediatric Asthma Study, a racially diverse birth cohort of 24,608 children born between 2000 and 2010 and insured by Kaiser Permanente Georgia. We estimated concentrations of mobile source fine particulate matter (PM2.5, µg/m), nitrogen oxides (NOX, ppb), and carbon monoxide (CO, ppm) at the maternal and child residence using a Research LINE source dispersion model for near-surface releases. Asthma was defined using diagnoses and medication dispensings from medical records. We used binomial generalized linear regression to model the impact of exposure continuously and by quintiles on asthma risk.\n\nRESULTS:\nControlling for covariates and modeling log-transformed exposure, a 2.7-fold increase in first year of life PM2.5 was associated with an absolute 4.1% (95% confidence interval, 1.6%, 6.6%) increase in risk of asthma by age 5. Quintile analysis showed an increase in risk from the first to second quintile, but similar risk across quintiles 2-5. Risk differences increased with follow-up age. Results were similar for NOX and CO and for exposure during pregnancy and the first year of life owing to high correlation.\n\nCONCLUSIONS:\nResults provide limited evidence for an association of early-life mobile source air pollution with childhood asthma incidence with a steeper concentration-response relationship observed at lower levels of exposure."
 },
 "questions": [
  {
   "id": "2054be89-feb5-4631-96dd-c5d471b29889",
   "text": "What are the risk factors of Asthma?",
   "answers": [
    {
     "answer_start": 1036,
     "text": "a 2.7-fold increase in first year of life PM2.5"
    },
    {
     "answer_start": 1387,
     "text": "NOX"
    },
    {
     "answer_start": 1395,
     "text": "CO"
    },
    {
     "answer_start": 1555,
     "text": "early-life mobile source air pollution"
    }
   ]
  }
 ]
}