Might Lifetime Exposure to Lead Confound the Association Between Hearing Impairment and Incident Dementia?

The methodologically rigorous study by Deal and colleagues, “Hearing Impairment and Incident Dementia and Cognitive Decline in Older Adults” (1), is an important contribution to the burgeoning evidence that hearing impairment (HI) is associated with increased risk of incident dementia (2). Deal and colleagues provide three potential mechanisms through which HI may be causally associated with dementia. However, the authors cautiously note that it “may be that both HI and dementia are caused by a common underlying pathology such as vascular disease.” ((1), p. 707) I hypothesize that lifetime exposure to lead may be an important “common underlying pathology” that is causally associated with both HI and dementia. To put the historic levels of lead exposure in context, it is helpful to compare levels found in the recent, well-publicized Flint Michigan drinking water crisis to those found in the 1970s before the complete phase-out of leaded gasoline. In Flint Michigan in 2014, tainted drinking water from corrosion in the lead pipes resulted in unacceptably high blood lead levels (BLL), with 5% of children under 6 years having BLL ≥5 µg/dL and 0.8% having BLL ≥10 µg/dL (3). In comparison, in the late 1970s, 99.8% of U.S. children under 6 years had BLL ≥5 µg/dL, 88.2% had BLL ≥10 µg/dL and 24.7% had BLL ≥20 µg/dL, with a mean for the whole U.S. population of 13.1 μg/dL (4), largely due to pollutants caused by tetraethyl lead additives in gasoline. Hearing loss has been linked to higher levels of blood (5,6) and bone (7) lead. In a population-based study of U.S. adolescents, the odds of high frequency hearing loss was double among those with BLL > 2 μg/dL in comparison to those with BLL < 1 μg/dL, even after many potential confounders were taken into account (5). In a study of lead battery workers in Iran, individuals with BLL between 10 and 19 μg/dL had triple the odds of high frequency hearing loss in comparison to those with BLL < 10 μg/dL (8). In a population-based U.S. sample, an exposure–response relationship was shown between level of BLL and HI, even after adjustments for other important risk factors for hearing loss (6). Cumulative lifetime exposure to lead, as measured by bone lead levels, is associated with higher odds of hearing loss and faster declines in hearing thresholds (7). Lifetime exposure to lead is also associated with accelerated cognitive decline in studies of occupationally exposed workers (9) and in a community cohort of nonoccupationally exposed older men (10,11). An expert panel funded by the National Institute of Health concluded that “sufficient evidence exists to conclude that there is an association between lead dose and decrements in cognitive function in adults.” ((9), p. 489). Experimental studies with animals have demonstrated that lead exposure can damage receptor cells in the inner ear, impair the function of auditory neurons (5–7), and increase amyloidogenesis and senile plaque deposition in primates (12). We have previously proposed that the unexpected substantial decline in the prevalence of HI in the U.S. adult population, aged 20–69, between 1999 and 2012 (13), and the dramatic decline in the incidence and age-adjusted prevalence of dementia in the developed world, may be partially due to lower lifetime lead exposure in later birth cohorts (14,15). A recent Lancet commissioned review (16), drawing upon the study by Deal et al. (1) among others, suggested that hearing loss is the leading preventable cause of dementia. This implies that the relationship between hearing loss and dementia is causal and therefore potentially modifiable with midlife management of hearing loss. An alternate plausible explanation is that lifetime exposure to the formerly ubiquitous neurotoxin, lead, may be causally associated with both hearing loss and dementia. In order to test this hypothesis, future studies examining the association between hearing loss and incident dementia could investigate whether adjustment for cumulative lifetime lead exposure, as measured by tibia bone lead level, substantially attenuates the hearing loss-dementia relationship. The author would like to gratefully acknowledge support received from the Sandra Rotman Endowed Chair in Social Work at the University of Toronto. None reported.

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