Associations between Air Pollution and Psychiatric Symptoms in The Normative Aging Study.

Background: Environmental risk factors for psychiatric health are poorly identified. We examined the association between air pollution and psychiatric symptoms, which are often precursors to the development of psychiatric disorders. Methods: This study included 570 participants in the US Veterans Administration (VA) Normative Aging Study and 1,114 visits (defined as an onsite follow-up at the VA with physical examination and questionnaires) from 2000-2014 with information on the Brief Symptom Inventory (BSI) to assess their psychiatric symptom levels. Differences in the three BSI global measures (Global Severity Index - GSI, Positive Symptom Distress Index - PSDI and Positive Symptom Total - PST) were reported per interquartile (IQR) increase of residential address-specific air pollutants levels (fine particulate matter - PM2.5, ozone - O3, nitrogen dioxide - NO2) at averages of 1 week, 4 weeks, 8 weeks and 1 year prior to the visit using generalized additive mixed effects models. We also evaluated modification by neighborhood factors. Results: On average, among the NAS sample (average age, 72.4 yrs. (standard deviation: 6.7 yrs.)), an IQR increase in 1- and 4- week averages of NO2 before visit was associated with a PSDI T score (indicator for psychiatric symptom intensity) increase of 1.60 (95% Confidence Interval (CI): 0.31, 2.89), 1.71 (95% CI: 0.18, 3.23), respectively. Similarly, for each IQR increase in 1- and 4-week averages of ozone before visit, PSDI T-score increased by 1.66 (95% CI: 0.68, 2.65), and 1.36 (95% CI: 0.23, 2.49), respectively. Stronger associations were observed for ozone and PSDI in low house value and low household income areas. No associations were found for PM2.5. Conclusions: Exposure to gaseous air pollutants was associated with higher intensity of psychiatric symptoms among a cohort of older men, particularly in communities with lower socio-economic or housing conditions.

Modifying effects of the HFE polymorphisms on the association between lead burden and cognitive decline.

BACKGROUND: As iron and lead promote oxidative damage, and hemochromatosis (HFE) gene polymorphisms increase body iron burden, HFE variant alleles may modify the lead burden and cognitive decline relationship. OBJECTIVE: Our goal was to assess the modifying effects of HFE variants on the lead burden and cognitive decline relation in older adults. METHODS: We measured tibia and patella lead using K-X-ray fluorescence (1991-1999) among participants of the Normative Aging Study, a longitudinal study of community-dwelling men from greater Boston. We assessed cognitive function with the Mini-Mental State Examination (MMSE) twice (1993-1998 and 1995-2000) and genotyped participants for HFE polymorphisms. We estimated the adjusted mean differences in lead-associated annual cognitive decline across HFE genotype groups (n = 358). RESULTS: Higher tibia lead was associated with steeper cognitive decline among participants with at least one HFE variant allele compared with men with only wild-type alleles (p interaction = 0.03), such that a 15 microg/g increase in tibia lead was associated with a 0.2 point annual decrement in MMSE score among HFE variant allele carriers. This difference in scores among men with at least one variant allele was comparable to the difference in baseline MMSE scores that we observed among men who were 4 years apart in age. Moreover, the deleterious association between tibia lead and cognitive decline appeared progressively worse in participants with increasingly more copies of HFE variant alleles (p-trend = 0.008). Results for patella lead were similar. CONCLUSION: Our findings suggest that HFE polymorphisms greatly enhance susceptibility to lead-related cognitive impairment in a pattern consistent with allelelic dose.