title: Climate change and its impact on allergic rhinitis and other allergic respiratory diseases.
abstract: OBJECTIVE
  To discuss current evidence of global climate change and its implications for allergic rhinitis and other allergic respiratory diseases.
  
  
  RESULTS
  Global climate change is evidenced by increasing average earth temperature, increasing anthropogenic greenhouse gas levels, and elevated pollen levels. Pollutants of interest include carbon dioxide (CO2), ozone (O3), and nitrous oxide (NO2) because they can enhance the allergic response and lead to increased symptoms of allergic respiratory diseases. Heightened CO2 levels stimulate pollen production via photosynthesis and increased growth in multiple plant species investigated. Although worsened air quality appears to increase prevalence of allergic rhinitis, the effects of increased temperature are less certain. The findings of increased aeroallergen levels likely contribute to increases in presentation of allergic diseases, although more healthcare impact studies are necessary.
  
  
  CONCLUSIONS
  Although recent literature indicates and strongly supports changes in temperature, pollution levels, and aeroallergen levels, more longitudinal epidemiologic surveillance of allergic diseases in relation to climate change as well as pathophysiologic studies on changing aeroallergen effects on allergic diseases are needed.
authors.affiliation: Department of Otolaryngology, University of Michigan Health Systems, Ann Arbor, Michigan, USA.
authors.forename: Giant C
authors.initials: GC
authors.lastname: Lin
authors.forename: Mark A
authors.initials: MA
authors.lastname: Zacharek
mesh_terms: D000393:Air Pollutants / Q000009:adverse effects; D057231:Climate Change; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D009297:Nasal Mucosa / Q000294:innervation; D009412:Nerve Fibers / Q000502:physiology; D020932:Nerve Growth Factor / Q000502:physiology; D009479:Neuropeptides / Q000502:physiology; D011159:Population Surveillance; D012130:Respiratory Hypersensitivity / Q000453:epidemiology* / Q000209:etiology* / Q000503:physiopathology; D012221:Rhinitis, Allergic, Perennial / Q000453:epidemiology* / Q000209:etiology* / Q000503:physiopathology; D006255:Rhinitis, Allergic, Seasonal / Q000453:epidemiology* / Q000209:etiology* / Q000503:physiopathology; D012636:Secretory Rate / Q000502:physiology; D011984:Sensory Receptor Cells / Q000502:physiology; D013373:Substance P / Q000502:physiology; D050916:TRPV Cation Channels / Q000502:physiology; D014660:Vasoactive Intestinal Peptide / Q000502:physiology
chemical_list: D000393:Air Pollutants; D018836:Inflammation Mediators; D009479:Neuropeptides; D050916:TRPV Cation Channels; C494482:TRPV1 protein, human; D013373:Substance P; D014660:Vasoactive Intestinal Peptide; D020932:Nerve Growth Factor