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Ascherio, Alberto

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Ascherio

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Alberto

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Ascherio, Alberto
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    Perinatal Air Pollutant Exposures and Autism Spectrum Disorder in the Children of Nurses’ Health Study II Participants
    (National Institute of Environmental Health Sciences, 2013) Roberts, Andrea L.; Lyall, Kristen; Hart, Jaime; Laden, Francine; Just, Allan C.; Bobb, Jennifer; Koenen, Karestan C.; Ascherio, Alberto; Weisskopf, Marc G.
    Objective: Air pollution contains many toxicants known to affect neurological function and to have effects on the fetus in utero. Recent studies have reported associations between perinatal exposure to air pollutants and autism spectrum disorder (ASD) in children. We tested the hypothesis that perinatal exposure to air pollutants is associated with ASD, focusing on pollutants associated with ASD in prior studies. Methods: We estimated associations between U.S. Environmental Protection Agency–modeled levels of hazardous air pollutants at the time and place of birth and ASD in the children of participants in the Nurses’ Health Study II (325 cases, 22,101 controls). Our analyses focused on pollutants associated with ASD in prior research. We accounted for possible confounding and ascertainment bias by adjusting for family-level socioeconomic status (maternal grandparents’ education) and census tract–level socioeconomic measures (e.g., tract median income and percent college educated), as well as maternal age at birth and year of birth. We also examined possible differences in the relationship between ASD and pollutant exposures by child’s sex. Results: Perinatal exposures to the highest versus lowest quintile of diesel, lead, manganese, mercury, methylene chloride, and an overall measure of metals were significantly associated with ASD, with odds ratios ranging from 1.5 (for overall metals measure) to 2.0 (for diesel and mercury). In addition, linear trends were positive and statistically significant for these exposures (p < .05 for each). For most pollutants, associations were stronger for boys (279 cases) than for girls (46 cases) and significantly different according to sex. Conclusions: Perinatal exposure to air pollutants may increase risk for ASD. Additionally, future studies should consider sex-specific biological pathways connecting perinatal exposure to pollutants with ASD.
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    Research on the Premotor Symptoms of Parkinson’s Disease: Clinical and Etiological Implications
    (National Institute of Environmental Health Sciences, 2013) Chen, Honglei; Burton, Edward A.; Ross, G. Webster; Huang, Xuemei; Savica, Rodolfo; Abbott, Robert D.; Ascherio, Alberto; Caviness, John N.; Gao, Xiang; Gray, Kimberly A.; Hong, Jau-Shyong; Kamel, Freya; Jennings, Danna; Kirshner, Annette; Lawler, Cindy; Liu, Rui; Miller, Gary W.; Nussbaum, Robert; Peddada, Shyamal D.; Rick, Amy Comstock; Ritz, Beate; Siderowf, Andrew D.; Tanner, Caroline M.; Tröster, Alexander I.; Zhang, Jing
    Background: The etiology and natural history of Parkinson’s disease (PD) are not well understood. Some non-motor symptoms such as hyposmia, rapid eye movement sleep behavior disorder, and constipation may develop during the prodromal stage of PD and precede PD diagnosis by years. Objectives: We examined the promise and pitfalls of research on premotor symptoms of PD and developed priorities and strategies to understand their clinical and etiological implications. Methods: This review was based on a workshop, Parkinson’s Disease Premotor Symptom Symposium, held 7–8 June 2012 at the National Institute of Environmental Health Sciences in Research Triangle Park, North Carolina. Discussion: Research on premotor symptoms of PD may offer an excellent opportunity to characterize high-risk populations and to better understand PD etiology. Such research may lead to evaluation of novel etiological hypotheses such as the possibility that environmental toxicants or viruses may initiate PD pathogenesis in the gastrointestinal tract or olfactory bulb. At present, our understanding of premotor symptoms of PD is in its infancy and faces many obstacles. These symptoms are often not specific to PD and have low positive predictive value for early PD diagnosis. Further, the pathological bases and biological mechanisms of these premotor symptoms and their relevance to PD pathogenesis are poorly understood. Conclusion: This is an emerging research area with important data gaps to be filled. Future research is needed to understand the prevalence of multiple premotor symptoms and their etiological relevance to PD. Animal experiments and mechanistic studies will further understanding of the biology of these premotor symptoms and test novel etiological hypothesis. Citation: Chen H, Burton EA, Ross GW, Huang X, Savica R, Abbott RD, Ascherio A, Caviness JN, Gao X, Gray KA, Hong JS, Kamel F, Jennings D, Kirshner A, Lawler C, Liu R, Miller GW, Nussbaum R, Peddada SD, Comstock Rick A, Ritz B, Siderowf AD, Tanner CM, Tröster AI, Zhang J. 2013. Research on the premotor symptoms of Parkinson’s Disease: clinical and etiological implications. Environ Health Perspect 121:1245–1252; http://dx.doi.org/10.1289/ehp.1306967
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    Particulate matter and risk of parkinson disease in a large prospective study of women
    (BioMed Central, 2014) Palacios, Natalia; Fitzgerald, Kathryn C.; Hart, Jaime; Weisskopf, Marc; Schwarzschild, Michael; Ascherio, Alberto; Laden, Francine
    Background: Exposure to air pollution has been implicated in a number of adverse health outcomes and the effect of particulate matter (PM) on the brain is beginning to be recognized. Yet, no prospective study has examined the association between PM and risk of Parkinson Disease. Thus, our goal was assess if exposure to particulate matter air pollution is related to risk of Parkinson’s disease (PD) in the Nurses’ Health Study (NHS), a large prospective cohort of women. Methods: Cumulative average exposure to different size fractions of PM up to 2 years before the onset of PD, was estimated using a spatio-temporal model by linking each individual’s places of residence throughout the study with location-specific air pollution levels. We prospectively followed 115,767 women in the NHS, identified 508 incident PD cases and used multivariable Cox proportional hazards models to estimate the risk of PD associated with each size fraction of PM independently. Results: In models adjusted for age in months, smoking, region, population density, caffeine and ibuprofen intake, we observed no statistically significant associations between exposure to air pollution and PD risk. The relative risk (RR) comparing the top quartile to the bottom quartile of PM exposure was 0.99 (95% Confidence Intervals (CI): 0.84,1.16) for PM10 (≤10 microns in diameter), 1.08 (95% CI: 0.81, 1.45) for PM2.5 (≤2.5 microns in diameter), and 0.92 (95% CI: 0.71, 1.19) for PM10–2.5 (2.5 to 10 microns in diameter). Conclusions: In this study, we found no evidence that exposure to air pollution is a risk factor for PD.
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    A Prospective Analysis of Airborne Metal Exposures and Risk of Parkinson Disease in the Nurses’ Health Study Cohort
    (NLM-Export, 2014) Palacios, Natalia; Fitzgerald, Kathryn C.; Roberts, Andrea L.; Hart, Jaime; Weisskopf, Marc; Schwarzschild, Michael; Ascherio, Alberto; Laden, Francine
    Background: Exposure to metals has been implicated in the pathogenesis of Parkinson disease (PD). Objectives: We sought to examine in a large prospective study of female nurses whether exposure to airborne metals was associated with risk of PD. Methods: We linked the U.S. Environmental Protection Agency (EPA)’s Air Toxics tract-level data with the Nurses’ Health Study, a prospective cohort of female nurses. Over the course of 18 years of follow-up from 1990 through 2008, we identified 425 incident cases of PD. We examined the association of risk of PD with the following metals that were part of the first U.S. EPA collections in 1990, 1996, and 1999: arsenic, antimony, cadmium, chromium, lead, manganese, mercury, and nickel. To estimate hazard ratios (HRs) and 95% CIs, we used the Cox proportional hazards model, adjusting for age, smoking, and population density. Results: In adjusted models, the HR for the highest compared with the lowest quartile of each metal ranged from 0.78 (95% CI: 0.59, 1.04) for chromium to 1.33 (95% CI: 0.98, 1.79) for mercury. Conclusions: Overall, we found limited evidence for the association between adulthood ambient exposure to metals and risk of PD. The results for mercury need to be confirmed in future studies. Citation: Palacios N, Fitzgerald K, Roberts AL, Hart JE, Weisskopf MG, Schwarzschild MA, Ascherio A, Laden F. 2014. A prospective analysis of airborne metal exposures and risk of Parkinson disease in the Nurses’ Health Study Cohort. Environ Health Perspect 122:933–938; http://dx.doi.org/10.1289/ehp.1307218
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    Indoor tanning bed use and risk of food addiction based on the modified Yale Food Addiction Scale
    (Editorial Department of Journal of Biomedical Research, 2017) Li, Wen-Qing; McGeary, John E.; Cho, Eunyoung; Flint, Alan; Wu, Shaowei; Ascherio, Alberto; Rimm, Eric; Field, Alison; Qureshi, Abrar A.
    Abstract The popularity of indoor tanning may be partly attributed to the addictive characteristics of tanning for some individuals. We aimed to determine the association between frequent indoor tanning, which we view as a surrogate for tanning addiction, and food addiction. A total of 67,910 women were included from the Nurses’ Health Study II. In 2005, we collected information on indoor tanning during high school/college and age 25-35 years, and calculated the average use of indoor tanning during these periods. Food addiction was defined as ≥3 clinically significant symptoms plus clinically significant impairment or distress, assessed in 2009 using a modified version of the Yale Food Addiction Scale. Totally 23.3% (15,822) of the participants reported indoor tanning at high school/college or age 25-35 years. A total of 5,557 (8.2%) women met the criteria for food addiction. We observed a dose–response relationship between frequency of indoor tanning and the likelihood of food addiction (Ptrend < 0.0001), independent of depression, BMI, and other confounders. Compared with never indoor tanners, the odds ratio (95% confidence interval) of food addiction was 1.07 (0.99-1.17) for average indoor tanning 1-2 times/year, 1.25 (1.09-1.43) for 3-5 times/year, 1.34 (1.14-1.56) for 6-11 times/year, 1.61 (1.35-1.91) for 12-23 times/year, and 2.98 (1.95-4.57) for 24 or more times/year. Frequent indoor tanning before or at early adulthood is associated with prevalence of food addiction at middle age. Our data support the addictive property of frequent indoor tanning, which may guide intervention strategies to curb indoor tanning and prevent skin cancer.
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    Genome-Wide Association Study of Circulating Vitamin D Levels
    (Oxford University Press, 2010) Ahn, Jiyoung; Yu, Kai; Stolzenberg-Solomon, Rachael; McCullough, Marjorie L.; Gallicchio, Lisa; Jacobs, Eric J.; Helzlsouer, Kathy; Jacobs, Kevin B.; Li, Qizhai; Weinstein, Stephanie J.; Purdue, Mark; Virtamo, Jarmo; Horst, Ronald; Chanock, Stephen; Hayes, Richard B.; Kraft, Peter; Albanes, Demetrius; Simon, Kelly Claire; Ascherio, Alberto; Wheeler, William; Hunter, David
    The primary circulating form of vitamin D, 25-hydroxy-vitamin D [25(OH)D], is associated with multiple medical outcomes, including rickets, osteoporosis, multiple sclerosis and cancer. In a genome-wide association study (GWAS) of 4501 persons of European ancestry drawn from five cohorts, we identified single-nucleotide polymorphisms (SNPs) in the gene encoding group-specific component (vitamin D binding) protein, GC, on chromosome 4q12-13 that were associated with 25(OH)D concentrations: rs2282679 (P = 2.0 × 10\(^{−30}\)), in linkage disequilibrium (LD) with rs7041, a non-synonymous SNP (D432E; P = 4.1 × 10\(^{−22}\)) and rs1155563 (P = 3.8 × 10\(^{−25}\)). Suggestive signals for association with 25(OH)D were also observed for SNPs in or near three other genes involved in vitamin D synthesis or activation: rs3829251 on chromosome 11q13.4 in NADSYN1 [encoding nicotinamide adenine dinucleotide (NAD) synthetase; P = 8.8 × 10\(^{−7}\)], which was in high LD with rs1790349, located in DHCR7, the gene encoding 7-dehydrocholesterol reductase that synthesizes cholesterol from 7-dehydrocholesterol; rs6599638 in the region harboring the open-reading frame 88 (C10orf88) on chromosome 10q26.13 in the vicinity of ACADSB (acyl-Coenzyme A dehydrogenase), involved in cholesterol and vitamin D synthesis (P = 3.3 × 10\(^{−7}\)); and rs2060793 on chromosome 11p15.2 in CYP2R1 (cytochrome P450, family 2, subfamily R, polypeptide 1, encoding a key C-25 hydroxylase that converts vitamin D3 to an active vitamin D receptor ligand; P = 1.4 × 10\(^{−5}\)). We genotyped SNPs in these four regions in 2221 additional samples and confirmed strong genome-wide significant associations with 25(OH)D through meta-analysis with the GWAS data for GC (P = 1.8 × 10\(^{−49}\)), NADSYN1/DHCR7 (P = 3.4 × 10\(^{−9}\)) and CYP2R1 (P = 2.9 × 10\(^{−17}\)), but not C10orf88 (P = 2.4 × 10\(^{−5}\)).
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    Overview of the Microbiome Among Nurses study (Micro-N) as an example of prospective characterization of the microbiome within cohort studies
    (Springer Science and Business Media LLC, 2021-04-21) Song, Mingyang; Everett, Christine; Li, Chengchen; Wilkinson, Jeremy; Nguyen, Long; McIver, Lauren; Ivey, Kerry; Izard, Jacques; Palacios, Natalia; Eliassen, A; Willett, Walter; Ascherio, Alberto; Sun, Qi; Tworoger, Shelley; Chang, Andrew; Garrett, Wendy; Huttenhower, Curtis; Rimm, Eric
    A lack of prospective studies has been a major barrier for assessing the role of the microbiome in human health and disease on a population-wide scale. To address this significant knowledge gap, we have launched a large-scale collection targeting fecal and oral microbiome specimens from 20,000 women within the Nurses’ Health Study II cohort (the Microbiome among Nurses, or Micro-N study). Leveraging the rich epidemiologic data that have been repeatedly collected from this cohort since 1989; the established biorepository of archived blood, urine, buccal cell, and tumor tissue specimens; the available genetic and biomarker data; the cohort's ongoing follow-up; and the BIOM-Mass microbiome research platform, Micro-N furnishes unparalleled resources for future prospective studies to interrogate the interplay between host, environmental factors, and the microbiome in human health. These prospectively collected materials will provide much-needed evidence to infer causality in microbiome-associated outcomes, paving the way towards development of microbiota-targeted modulators, preventives, diagnostics and therapeutics. Here, we describe a generalizable, scalable and cost-effective platform used for stool and oral microbiome specimen and metadata collection in the Micro-N study as an example of how prospective studies of the microbiome may be carried out.
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    Air Pollution and Risk of Parkinson’s Disease in a Large Prospective Study of Men
    (Environmental Health Perspectives, 2017) Palacios, Natalia; Fitzgerald, Kathryn C.; Hart, Jaime; Weisskopf, Marc; Schwarzschild, Michael; Ascherio, Alberto; Laden, Francine
    Background: Exposure to air pollution has been implicated in a number of adverse health outcomes, and the effect of particulate matter (PM) on the brain is beginning to be recognized. Objectives: We aimed to examine whether exposure to PM air pollution is related to risk of Parkinson's disease (PD) in the Health Professionals Follow-up Study (HPFS), a large prospective cohort of U.S. men. Methods: We prospectively followed 50,352 men in the HPFS, a large prospective cohort of U.S. men, and identified 550 incident PD cases. Cumulative average exposure to various size fractions of PM [PM10 (≤10μm microns in diameter), PM2.5 (≤2.5μm in diameter), and PM2.5–10 (between 2.5 and 10μm in diameter)] up to 2 years before the onset of PD was estimated using a spatiotemporal model by linking each participant’s place of residence throughout the study with location-specific PM levels. We used multivariable Cox proportional hazards models to independently estimate the risk of PD associated with each size fraction of PM. Results: In models adjusted for age, smoking, region, and population density, we did not observe statistically significant associations between exposure to PM and PD risk. In analyses considering cumulative average PM exposure, the comparing the top to the bottom quintile of PM exposure was 0.85 [95% confidence interval (CI): (0.63, 1.15)] for PM10, 0.97 [95% CI: (0.72, 1.32)] for PM2.5, and 0.88 [95% CI: (0.64, 1.22)] for hazard ratio (HR) PM2.5–10. The results did not change markedly when restricted to men who did not move during the study or when stratified by smoking status or population density. Conclusions: In this study, we found no evidence that exposure to air pollution is a risk factor for PD in men. https://doi.org/10.1289/EHP259