HEALTH RISK-EVALUATION OF NITROGEN-OXIDES

Citation
M. Berglund et al., HEALTH RISK-EVALUATION OF NITROGEN-OXIDES, Scandinavian journal of work, environment & health, 19, 1993, pp. 1-72
Citations number
454
Categorie Soggetti
Ergonomics,"Public, Environmental & Occupation Heath
ISSN journal
03553140
Volume
19
Year of publication
1993
Supplement
2
Pages
1 - 72
Database
ISI
SICI code
0355-3140(1993)19:<1:HRON>2.0.ZU;2-T
Abstract
The nitrogen oxides discussed in this document are nitric oxide (NO) a nd nitrogen dioxide (NO2). In combustion processes, NO is primarily fo rmed and subsequently oxidized to NO2 in the atmosphere. Traffic is th e major source to human outdoor exposure to NO and NO2 in urban areas. In homes with gas-fueled stoves or water heaters, the concentration o f NO2 is generally higher indoors than outdoors. Upon inhalation, NO2 penetrates deep into the lung. In animal experiments, NO2 causes bioch emical and morphological changes in lung tissue, affects host defense mechanisms, and causes decreased pulmonary function. The lowest observ ed effect level after prolonged exposure is 560 mug.m-3. In short-term controlled studies on humans, NO2 causes bronchoconstriction and an i ncrease in bronchial responsiveness. A meta-analysis indicates a lowes t observed effect level of 200 mug.m-3 for increased bronchial respons iveness in asthmatics. Epidemiologic studies on children living in hom es with gas stoves suggest an increased risk of lower respiratory illn ess at average indoor NO2 concentrations of about 40-80 mug.m-3, with short-term peaks exceeding 1000 mug.m-3. The studies focusing on outdo or exposure provide some evidence of increased respiratory disease rat es for children and nonsmoking adults living in areas with long-term a verage NO2 concentrations of 30-100 mug.m-3; however, the specific rol e of NO2 is not clear. Based on controlled studies on humans, a 1-h gu ideline value of 100 mug.m-3 for NO2 in ambient air (eg, as the 99th p ercentile) is recommended. This value would correspond to a long-term average (half-year mean) of about 40 mug.m-1. The epidemiologic eviden ce is not considered sufficient for a long-term guideline for NO2. NO is formed endogenously for purposes such as signaling in the nervous s ystem, the mediation of vasodilation, and the mediation of cytotoxicit y in macrophages. After the inhalation of high concentrations of NO, l ung vasodilator effects occur. No health-based guideline value for NO in ambient air is suggested.