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A novel hypothesis to explain traffic-related nocturnal cough
- Peter M. Joseph, none (19 December 2007)
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Peter M. Joseph, Professor University of Pennsylvania, none
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joseph{at}rad.upenn.edu Peter M. Joseph, et al.
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I am writing to comment on the paper[1] by Morgenstern et al. entitled “Respiratory health and individual estimated exposure to traffic-related air pollutants in a cohort of young children” The paper looked at the health effects of various components of air pollution as they depended on distance from major traffic arteries in and around Munich, Germany. I do not disagree with the data of that paper, which was obtained in a highly competent fashion. Rather, I want to suggest a novel hypothesis that might help to explain the results.
The key finding I want to examine is the observed association of ambient NO2 levels and nocturnal cough in very young children. Morgenstern’s Table 4 shows that NO2 concentrations (a misprint in the units) varied from 19.4 to 71.7 ìg/m3, with a mean of 35.4. Those concentrations are much lower than those that have been demonstrated to have harmful effects, at least in adults. According to one authoritative review[2] there is little evidence that NO2 has any respiratory effect, even on asthmatics, at concentrations less than 200 ppb (376 ìg/m3 ). An excellent review[3] of the health effects of outdoor NO2 concluded:. “The overall results suggest that outdoor NO2 was serving as a marker for more causal agents ...” That conclusion obviously suggests that there may be a missing (unknown) pollutant that can, in some circumstances, mimic NO2 in ecological studies. Other environmental epidemiologists have expressed the suspicion that some effects associated with criterion pollutants may instead be due to unmeasured confounding pollutants[4]. One paper[5] specifically suggested that the observed association of children’s symptoms with NO2 could mean that the NO2 was a marker for other components of vehicular exhaust. The idea that NO2 may have harmful effects on young children is not new. However, the existing literature could be described as conflicting[6], with one study[7] of indoor NO2 at concentrations in the range 60-300 ìg/m3 finding no effect in children aged 6-9 years. I found several papers that found no such association, including four that looked at infants[8-11]. These results make it unlikely that NO2 itself was the direct cause of the cough. Since the cough was seen only at night, we should think of a pollutant whose concentrations are larger at night than in daytime. We are not aware of any diurnal data on NO2 in Munich. However, studies in California[12 13], Finland[14], Stuttgart[15], and Rome[16] indicate that daytime concentrations are generally larger than those seen late at night. That result is comprehensible for two reasons: (1) In most cities traffic density is much less at night than in daytime, and (2) the production of NO2 from NO is greatly accelerated by ozone in the air, which is maximal in daytime. I know of no urban study indicating that NO2 is primarily a nocturnal pollutant. For several years I have argued that methyl nitrite (MN) is an important but unrecognized exhaust component of engines with methyl ether (such as MTBE) in the fuel[17]. MN has the very unusual property that it is rapidly destroyed by photolysis from sunlight[18]. Photolysis[19 20] of MN produces NO, which is naturally oxidized to NO2 by sunlight. These facts have two immediate consequences: (1) on most (sunny) days MN will be a strictly nocturnal pollutant, and (2) on sunny mornings NO2 will be a marker for MN of the previous night. MN is stable in night air[21]. Hence MN has exactly the properties that might explain the apparent association of NO2 with nocturnal cough. Readers wishing to learn more about MN might want to read my recent paper[22]entitled “Paradoxical Ozone Associations could be due to Methyl Nitrite from Combustion of Methyl Ethers or Esters in Engine Fuels”. That paper focused on several ozone studies that, inexplicably, found negative associations of ozone with morbidity, especially for asthma in children[23 24]. I argued that MN has exactly the properties needed to explain those associations, and may also explain a large part of the increase in asthma prevalence seen in the US over the period 1980-2000. I want to thank Dr. Joachim Heinrich for recently bringing the Morgenstern paper to my attention.
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