Are Males More Susceptible To Ambient PM Than Females?
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Recent epidemiologic studies of modern air pollution show statistically significant relationships between fluctuations of daily non-trauma mortality and fluctuations of daily ambient particulate matter (PM) levels at low concentrations. A review of historic smoke-fog (smog)episodes (Meuse Valley, Donora, London)was conducted to seek common characteristics of victims of higher concentrations of ambient PM to help identify a susceptible cohort for an effect at lower ambient PM concentrations. The Meuse Valley episode investigation (Firket, 1931) did not detail the age and sex of the victims, so we obtained complete death certificates from all the Belgian villages in the area over the period of the smog (December 1 - 7, 1930), and these data on gender and age are reported here for the first time. The results show a -50% excess male death rate 36, 25 consistent with the previously reported excess male deaths in both the Donora Fog 15, 5 and the London Fog autopsies cases, 419,287. In all three episode, mortality was predominantly amongst the aged, and most of those autopsied presented with pre-existing cardiopulmonary lesions.
Because the genders, ages and smoking habits of the populations-at-risk were unrecorded, we are unable to adjust for an expectation of more aged females and higher male smoking rates. However, recent studies of PM and mortality have found no statically significant different risk for smokers and no-smokers (Pope et al., 1995). We present data on other causes of death that also have a 50% male excess death rate. We test an X-linkage genetic model that explains the -50% excess male death rate using total U.S. infant mortality data and data on suicides by gas in Paris, and the model cannot be rejected as a reasonable fit. The findings of this study support the hypothesis that males are genetically more susceptible to the effected of ambient PM exposures.
Because the genders, ages and smoking habits of the populations-at-risk were unrecorded, we are unable to adjust for an expectation of more aged females and higher male smoking rates. However, recent studies of PM and mortality have found no statically significant different risk for smokers and no-smokers (Pope et al., 1995). We present data on other causes of death that also have a 50% male excess death rate. We test an X-linkage genetic model that explains the -50% excess male death rate using total U.S. infant mortality data and data on suicides by gas in Paris, and the model cannot be rejected as a reasonable fit. The findings of this study support the hypothesis that males are genetically more susceptible to the effected of ambient PM exposures.