2. Marco teórico
2.5 Planificación Estratégica en el Sector Público
The concept of scarring was used in a study by Preston, Hill, and Drevenstedt (1998) that examines the relationship between early life conditions and survival to ages over 85 in a population of African Americans. Arguing that their sample of decedents over age 85 was representative of all those alive over that age, they use records linkage from death records to the 1900 and 1910 US censuses to determine socioeconomic characteristics in childhood. They posit four possible ways through which childhood conditions could be related to adult mortality: positive (childhood infection leads to higher mortality) and negative (childhood infection leads to lower mortality), both with direct and indirect possibilities. Their research supports the direct effects, the scarring (positive) and acquired immunity (negative) hypotheses, but not the argument concerning indirect effects (however, their sample necessarily precludes those who died before the age of 85). Acquired immunity may explain why older adult mortality was low, but does not adequately describe why young adult mortality was so high, only in 1918.
Scarring offers a plausible explanation. Preston and colleagues state that “certain conditions and diseases acquired in childhood may, in a sense, permanently impair the survivors and leave an imprint on death rates at all subsequent ages,” using the examples of tuberculosis, hepatitis B and rheumatic heart disease (1998:1232). With historical data from Sweden, Bengtsson and Lindstrӧm (2003) found that “airborne infectious diseases are important for the causal mechanisms linking infant mortality to old-age (55-80 years) mortality” (2003:293) such that “children severely exposed to airborne infectious diseases during their birth year had a much higher risk of dying of airborne infectious diseases in their old age” (2003:286). The mechanism through which the relationship between exposure to severe respiratory illness in childhood and higher mortality in later life actually occurs is less well developed. Bengtsson and Lindstrӧm (2003) argue that there is no medical evidence for the suggestion by Fridlizius (1989) that “diseases during the first years of life would affect survival during adulthood through an irreversible damaging effect on the immunological system” (2003:292) (however, c.f. Section 2.4.3). Yet, they report that respiratory infections in the first year of life have been shown to be associated with morbidity and mortality from “cough, phlegm, and impaired ventilator
function” as well as “early bronchitis and pneumonia” providing “evidence of persistent lung damage from respiratory infectious disease during the first year of life” (2003:292). Therefore it is assumed in this dissertation for the scarring mechanism that infection early in life from a severe respiratory infectious disease (the 1890 influenza) causes physiological damage which impairs survival from another severe respiratory infection in later life.
Infection with influenza can lead to lasting physiological impairments. As previously mentioned, the 1890 Russian influenza was thought to impact the innervation of the heart, meaning that the flu left those who had survived it with nerve damage to their essential organs (Legislative Assembly of Ontario 1896, Horder 1918). This nerve damage may also lead to encephalopathy and encephalitis, and manic psychosis (Glezen and Couch 1997, Honigsbaum 2010). Epidemics of encephalitis lethargica and Parkinson’s disease have been proposed as being sequelae of influenza infection (Ravenholt and Foege 1892) and neurological effects have been reported for more recent influenza epidemics (Delorme and Middleton 1979, Fujimoto et al. 1998, Toovey 2008, Baltagi et al. 2010, Chen et al. 2010, Shah et al. 2013). Direct damage to the lungs has also been found (Doblhammer 2004). Laraya-Cuasay and colleagues found that “influenza virus infection may be more serious in infants and young children than has been previously recognized and may contribute to the pathogenesis of unexplained interstitial pneumonitis, pulmonary fibrosis, obliterative bronchiolitis, and bronchiectasis” (1977:617). Further, it was found that “asymptomatic mechanical dysfunction of the lungs is a frequent sequela to acute influenza A virus infection” (Hall et al. 1976:141). Therefore, it is medically plausible that infection with a severe respiratory infection in childhood could lead to later respiratory impairments. These sequelae are not common however (Wang et al. 2010), meaning that it becomes difficult to assert that every individual who contracted the 1890 influenza was subject to this process. Individualized morbidity records and prospective tracking of individuals to the time of death would be a better means to investigate this process. The results from using age at death alone to research this process must therefore be interpreted with caution.
In terms of the relationship between the 1890 and 1918 pandemics, I hypothesize that infection with the Russian pandemic early in life may have damaged lung tissue, placing individuals at risk either for infection with any airborne infectious disease encountered later in life (including the 1918 flu), or specifically to the extreme sequelae resulting from secondary bacterial infection in 1918. There were many airborne infectious diseases circulating in Ontario between 1890 and 1918, including (among others) diphtheria, measles, smallpox, tuberculosis, typhoid fever, and whooping cough. Scarring could have been caused by any of these diseases (both before and after 1890) and would have placed individuals at greater risk from all following infections. For this reason, this mechanism through which early life exposure has an impact on mortality in later life is more speculative and more difficult to assert.
The examination of the scarring hypothesis for these two pandemics must take into account selection biases. It is possible that those individuals who were the most severely scarred in 1890 would have been more susceptible to contracting and dying from an airborne infectious disease between 1890 and 1918. Therefore, the individuals who are of greatest interest would not have survived to be included in the sample. If scarring did affect mortality in 1918, it could be seen in a concentration of deaths among individuals born in 1889, or those who were alive to experience the epidemic for themselves. For those individuals who were breastfeeding at the time and therefore benefiting from their mothers immune system, deaths in 1918 would be expected to be greatest for those exposed to the flu at the time of weaning (or approximately between the ages of 3 and 6 months, when breast milk is no longer sufficient as a sole food source. Timing varies slightly by ethnic and religious origins, Wharton 1989, Hendricks and Badruddin 1992). Infants who were not breastfeeding, and older children, would have been vulnerable to the effects of scarring throughout the period of the epidemic.20 As such, it will likely be
20
It is difficult to get a depiction of common breastfeeding practices in Ontario from 1883-1895. There was a large movement in the 1910s in Ontario focusing on reducing infant mortality, following precedents set in the United States and Britain (Chapin 1921, Piva 1979, MacDougall 1990, Comacchio 1992, Hallman 2009). The imposition of well- baby clinics and milk stations throughout Toronto may indicate that breastfeeding was not widespread during this later period, at least in the cities and among the impoverished. However, at this time there was no reliably sufficient substitute for breast milk, the quality of cow milk was poor, and the water used to clean bottles was often unsafe, such that many bottle-fed babies died (Meckel 1990, Comacchio 1992). MacMurchy notes this in her 1910 report on infant
difficult to separate the exact mechanisms that may have occurred for individuals who were alive during the epidemic (scarring and antigenic imprinting). However, gestational effects would be more likely to have been the main mechanisms for individuals whose exposure occurred in utero.