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Modification by hemochromatosis gene polymorphisms of the association between traffic-related air pollution and cognition in older men: a cohort study.

ABSTRACT: Previous studies found effect modification of associations between traffic-related air pollution and cardiovascular outcomes by polymorphisms in the hemochromatosis gene (HFE). As traffic-related air pollution may impact cognition through effects on cardiovascular health or through mechanisms which may also influence cardiovascular outcomes, we hypothesized that HFE polymorphisms would also modify a previously observed association between traffic-related air pollution exposure and cognition in older men.We considered data from 628 participants of the VA Normative Aging Study. We estimated long term exposure to black carbon (BC), a marker of traffic related air pollution, using a spatio-temporal land use regression model. We assessed cognition using the Mini-Mental State Examination (MMSE), a test of global function, and performance on a battery of other tests, covering a wide range of domains. We investigated whether variants of HFE C282Y and H63D modified the association between BC and having a low MMSE score using logistic models with generalized estimating equations and multiplicative interaction terms. Similarly, we assessed whether HFE variants modified the association between BC and performance on the cognitive battery using linear mixed models with multiplicative interaction terms.Our results suggest modification of the BC-cognition association by HFE C282Y, although the test of interaction did not achieve statistical significance. In multivariable-adjusted models, participants who lacked a HFE C282Y variant (CC) exhibited an adverse association between BC and total cognition z-score (beta for a doubling in BC concentration: -0.061, 95% CI: -0.115, -0.007), while we did not observe an association in participants with at least one variant genotype (CY or YY) (beta for a doubling in BC concentration: 0.073, 95% CI: -0.081, 0.228; p-value for interaction: 0.11). The pattern of association was similar for analyses considering performance on the Mini-Mental State Examination. There was little evidence to support effect modification of the BC-cognition association by the HFE H63D genotype.Our data suggest that older adults who lack an HFE C282Y variant may be more susceptible to an adverse effect of traffic-related air pollution exposure on cognition. This finding and the proposed biological mechanism require confirmation.

SUBMITTER: Power MC

PROVIDER: S-EPMC3599892 | biostudies-literature | 2013 Feb

REPOSITORIES: biostudies-literature

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Modification by hemochromatosis gene polymorphisms of the association between traffic-related air pollution and cognition in older men: a cohort study.

Power Melinda C MC Weisskopf Marc G MG Alexeeff Stacey E SE Wright Robert O RO Coull Brent A BA Spiro Avron A Schwartz Joel J

Environmental health : a global access science source 20130215

<h4>Background</h4>Previous studies found effect modification of associations between traffic-related air pollution and cardiovascular outcomes by polymorphisms in the hemochromatosis gene (HFE). As traffic-related air pollution may impact cognition through effects on cardiovascular health or through mechanisms which may also influence cardiovascular outcomes, we hypothesized that HFE polymorphisms would also modify a previously observed association between traffic-related air pollution exposure ...[more]

PMID: 23413885

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Project description:Acute exposure to ambient air pollution has been associated with acute changes in cardiac outcomes, often within hours of exposure.We examined the effects of air pollutants on heart-rate-corrected QT interval (QTc), an electrocardiographic marker of ventricular repolarization, and whether these associations were modified by participant characteristics and genetic polymorphisms related to oxidative stress.We studied repeated measurements of QTc on 580 men from the Veterans Affairs Normative Aging Study (NAS) using mixed-effects models with random intercepts. We fitted a quadratic constrained distributed lag model to estimate the cumulative effect on QTc of ambient air pollutants including fine particulate matter <or= 2.5 microm in aerodynamic diameter (PM2.5), ozone (O3), black carbon (BC), nitrogen dioxide (NO2), carbon monoxide (CO), and sulfur dioxide (SO2) concentrations during the 10 hr before the visit. We genotyped polymorphisms related to oxidative stress and analyzed pollution-susceptibility score interactions using the genetic susceptibility score (GSS) method.Ambient traffic pollutant concentrations were related to longer QTc. An interquartile range (IQR) change in BC cumulative during the 10 hr before the visit was associated with increased QTc [1.89 msec change; 95% confidence interval (CI), -0.16 to 3.93]. We found a similar association with QTc for an IQR change in 1-hr BC that occurred 4 hr before the visit (2.54 msec change; 95% CI, 0.28-4.80). We found increased QTc for IQR changes in NO2 and CO, but the change was statistically insignificant. In contrast, we found no association between QTc and PM2.5, SO2, and O3. The association between QTc and BC was stronger among participants who were obese, who had diabetes, who were nonsmokers, or who had higher GSSs.Traffic-related pollutants may increase QTc among persons with diabetes, persons who are obese, and nonsmoking elderly individuals; the number of genetic variants related to oxidative stress increases this effect.

Project description:ObjectiveTo investigate associations between long term residential exposure to road traffic noise and particulate matter with a diameter <2.5 µm (PM2.5) and infertility in men and women.DesignNationwide prospective cohort study.SettingDenmark.Participants526 056 men and 377 850 women aged 30-45 years, with fewer than two children, cohabiting or married, and residing in Denmark between 2000 and 2017.Main outcome measureIncident infertility in men and women during follow-up in the Danish National Patient Register.ResultsInfertility was diagnosed in 16 172 men and 22 672 women during a mean follow-up of 4.3 years and 4.2 years, respectively. Mean exposure to PM2.5 over five years was strongly associated with risk of infertility in men, with hazard ratios of 1.24 (95% confidence interval 1.18 to 1.30) among men aged 30-36.9 years and 1.24 (1.15 to 1.33) among men aged 37-45 years for each interquartile (2.9 µg/m3) higher PM2.5 after adjustment for sociodemographic variables and road traffic noise. PM2.5 was not associated with infertility in women. Road traffic noise (Lden, most exposed facade of residence) was associated with a higher risk of infertility among women aged 35-45 years, with a hazard ratio of 1.14 (1.10 to 1.18) for each interquartile (10.2 dB) higher five year mean exposure. Noise was not associated with infertility among younger women (30-34.9 years). In men, road traffic noise was associated with higher risk of infertility in the 37-45 age group (1.06, 1.02 to 1.11), but not among those aged 30-36.9 years (0.93, 0.91 to 0.96).ConclusionsPM2.5 was associated with a higher risk of an infertility diagnosis in men, whereas road traffic noise was associated with a higher risk of an infertility diagnosis in women older than 35 years, and potentially in men older than 37 years. If these results are confirmed in future studies, higher fertility could be added to the list of health benefits from regulating noise and air pollution.

Project description:Physical disability is common though not inevitable in older age and has direct bearing on a person's ability to perform activities essential for self-care and independent living. Air pollution appears to increase the risk of several chronic diseases that contribute to the progression of disability.We evaluated long-term exposure to traffic-related air pollution (TRAP) in relation to progression in physical disability.We conducted our investigation within the Chicago Health and Aging Project. We measured participants' exposures to TRAP using two surrogates: residential proximity to major roads (1993 onwards) and ambient concentrations of oxides of nitrogen (NOX; 1999 onwards), predicted via a geographic information systems-based spatiotemporal smoothing model (cross-validation R2 = 0.87) that incorporated community-based monitoring and resolved intraurban exposure gradients at a spatial scale of tens of meters. Participants' lower-extremity physical ability was assessed every 3 years (1993-2012) via tandem stand, chair stand, and timed walking speed.In multivariable-adjusted analyses (n = 5,708), higher long-term NOX exposure was associated with significantly faster progression in disability. Compared with the 5-year decline in physical ability score among participants in the lowest quartile of NOX exposure, decline among those in the highest exposure quartile was 1.14 units greater (95% confidence interval [CI]: -1.86, -0.42), equivalent to 3 additional years of decline among those in the lowest exposure quartile. The association was linear across the continuum of NOX exposure: per 10-ppb increment in exposure, the 5-year decline in physical ability score was 0.87 unit greater (95% CI: -1.35, -0.39). Proximity to a major road was not associated with disability progression (n = 9,994).These data join a growing body of evidence suggesting that TRAP exposures may accelerate aging-related declines in health.Weuve J, Kaufman JD, Szpiro AA, Curl C, Puett RC, Beck T, Evans DA, Mendes de Leon CF. 2016. Exposure to traffic-related air pollution in relation to progression in physical disability among older adults. Environ Health Perspect 124:1000-1008;?http://dx.doi.org/10.1289/ehp.1510089.

Project description:Autism is a heterogeneous disorder with genetic and environmental factors likely contributing to its origins. Examination of hazardous pollutants has suggested the importance of air toxics in the etiology of autism, yet little research has examined its association with local levels of air pollution using residence-specific exposure assignments.To examine the relationship between traffic-related air pollution, air quality, and autism.This population-based case-control study includes data obtained from children with autism and control children with typical development who were enrolled in the Childhood Autism Risks from Genetics and the Environment study in California. The mother's address from the birth certificate and addresses reported from a residential history questionnaire were used to estimate exposure for each trimester of pregnancy and first year of life. Traffic-related air pollution was assigned to each location using a line-source air-quality dispersion model. Regional air pollutant measures were based on the Environmental Protection Agency's Air Quality System data. Logistic regression models compared estimated and measured pollutant levels for children with autism and for control children with typical development.Case-control study from California.A total of 279 children with autism and a total of 245 control children with typical development.Crude and multivariable adjusted odds ratios (AORs) for autism.Children with autism were more likely to live at residences that had the highest quartile of exposure to traffic-related air pollution, during gestation (AOR, 1.98 [95% CI, 1.20-3.31]) and during the first year of life (AOR, 3.10 [95% CI, 1.76-5.57]), compared with control children. Regional exposure measures of nitrogen dioxide and particulate matter less than 2.5 and 10 ?m in diameter (PM2.5 and PM10) were also associated with autism during gestation (exposure to nitrogen dioxide: AOR, 1.81 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.08 [95% CI, 1.93-2.25]; exposure to PM10: AOR, 2.17 [95% CI, 1.49-3.16) and during the first year of life (exposure to nitrogen dioxide: AOR, 2.06 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.12 [95% CI, 1.45-3.10]; exposure to PM10: AOR, 2.14 [95% CI, 1.46-3.12]). All regional pollutant estimates were scaled to twice the standard deviation of the distribution for all pregnancy estimates.Exposure to traffic-related air pollution, nitrogen dioxide, PM2.5, and PM10 during pregnancy and during the first year of life was associated with autism. Further epidemiological and toxicological examinations of likely biological pathways will help determine whether these associations are causal.

Project description:BackgroundA recent meta-analysis suggested evidence for an effect of exposure to ambient air pollutants on risk of certain congenital heart defects. However, few studies have investigated the effects of traffic-related air pollutants with sufficient spatial accuracy.ObjectivesWe estimated associations between congenital anomalies and exposure to traffic-related air pollution in Barcelona, Spain.MethodCases with nonchromosomal anomalies (n = 2,247) and controls (n = 2,991) were selected from the Barcelona congenital anomaly register during 1994-2006. Land use regression models from the European Study of Cohorts for Air Pollution Effects (ESCAPE), were applied to residential addresses at birth to estimate spatial exposure to nitrogen oxides and dioxide (NOx, NO2), particulate matter with diameter ? 10 ?m (PM10), 10-2.5 ?m (PMcoarse), ? 2.5 ?m (PM2.5), and PM2.5 absorbance. Spatial estimates were adjusted for temporal trends using data from routine monitoring stations for weeks 3-8 of each pregnancy. Logistic regression models were used to calculate odds ratios (ORs) for 18 congenital anomaly groups associated with an interquartile-range (IQR) increase in exposure estimates.ResultsIn spatial and spatiotemporal exposure models, we estimated statistically significant associations between an IQR increase in NO2 (12.2 ?g/m3) and coarctation of the aorta (ORspatiotemporal = 1.15; 95% CI: 1.01, 1.31) and digestive system defects (ORspatiotemporal = 1.11; 95% CI: 1.00, 1.23), and between an IQR increase in PMcoarse (3.6 ?g/m3) and abdominal wall defects (ORspatiotemporal = 1.93; 95% CI: 1.37, 2.73). Other statistically significant increased and decreased ORs were estimated based on the spatial model only or the spatiotemporal model only, but not both.ConclusionsOur results overall do not indicate an association between traffic-related air pollution and most groups of congenital anomalies. Findings for coarctation of the aorta are consistent with those of the previous meta-analysis.CitationSchembari A, Nieuwenhuijsen MJ, Salvador J, de Nazelle A, Cirach M, Dadvand P, Beelen R, Hoek G, Basagaña X, Vrijheid M. 2014. Traffic-related air pollution and congenital anomalies in Barcelona. Environ Health Perspect 122:317-323;?http://dx.doi.org/10.1289/ehp.1306802.

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Project description:PurposeTo investigate the association between exposure to traffic-related air pollution and use of spectacles (as a surrogate measure for myopia) in schoolchildren.MethodsWe analyzed the impact of exposure to NO2 and PM2.5 light absorbance at home (predicted by land-use regression models) and exposure to NO2 and black carbon (BC) at school (measured by monitoring campaigns) on the use of spectacles in a cohort of 2727 schoolchildren (7-10 years old) in Barcelona (2012-2015). We conducted cross-sectional analyses based on lifelong exposure to air pollution and prevalent cases of spectacles at baseline data collection campaign as well as longitudinal analyses based on incident cases of spectacles use and exposure to air pollution during the three-year period between the baseline and last data collection campaigns. Logistic regression models were developed to quantify the association between spectacles use and each of air pollutants adjusted for relevant covariates.ResultsAn interquartile range increase in exposure to NO2 and PM2.5 absorbance at home was respectively associated with odds ratios (95% confidence intervals (CIs)) for spectacles use of 1.16 (1.03, 1.29) and 1.13 (0.99, 1.28) in cross-sectional analyses and 1.15 (1.00, 1.33) and 1.23 (1.03, 1.46) in longitudinal analyses. Similarly, odds ratio (95% CIs) of spectacles use associated with an interquartile range increase in exposures to NO2 and black carbon at school was respectively 1.32 (1.09, 1.59) and 1.13 (0.97, 1.32) in cross-sectional analyses and 1.12 (0.84, 1.50) and 1.27 (1.03, 1.56) in longitudinal analyses. These findings were robust to a range of sensitivity analyses that we conducted.ConclusionWe observed increased risk of spectacles use associated with exposure to traffic-related air pollution. These findings require further confirmation by future studies applying more refined outcome measures such as quantified visual acuity and separating different types of refractive errors.

Dataset Information

Modification by hemochromatosis gene polymorphisms of the association between traffic-related air pollution and cognition in older men: a cohort study.

Publications

Modification by hemochromatosis gene polymorphisms of the association between traffic-related air pollution and cognition in older men: a cohort study.

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