Publications
13 results found
Laine J, Huybrechts I, Gunter M, et al., 2021, Co-benefits from sustainable dietary shifts for population and environmental health: an assessment from a large European cohort study, The Lancet Planetary Health, Vol: 5, Pages: e786-e796, ISSN: 2542-5196
Background: Unhealthy diets, the rise of non-communicable diseases, and the declining health of the planet are highly intertwined, where food production and consumption are major drivers of increases in greenhouse gas (GHG) emissions, substantial land use, (LU) and adverse health outcomes such as cancer and mortality. Methods: In the European Prospective Investigation into Cancer and Nutrition (EPIC), a multi-centre prospective cohort study (n=443,991), we estimated associations between dietary contributions to GHG emissions and LU and all-cause and cause-specific mortality and incident cancers using Cox proportional-hazard regression models. Co-benefits, encompassing the potential effects of alternative diets on all-cause mortality and cancer and potential reduction in GHG emissions and LU, were estimated using counterfactual attributable fraction (AF) intervention models, simulating potential effects from dietary shifts based on the EAT-Lancet reference diet. Findings: There was an association between levels of dietary-based GHG emissions and LU and all-cause mortality, with a Hazard Ratio and 95% Confidence Interval (CI) of 1.13 (1.10, 1.16) and 1.18 (95% CI: 1.15, 1.21), respectively, comparing the fourth quartile to the first (HRQ4 vs Q1). Similar associations were observed for cause-specific mortality. There were also associations between overall cancer rates and GHG emissions (HRQ4 vs Q1: 1.11, 95% CI: 1.09, 1.14) and LU (HRQ4 vs Q1: 1.13, 95% CI: 1.10, 1.15); however, estimates differed by cancer type. Through counterfactual AF modelling of shifts in diets, we find that between 19 to 63% of deaths and 10 to 39% of cancers could be prevented, over a 20-year risk period, from adhering to different scores of the EAT-Lancet reference diet. Additionally, switching from a lower score of the EAT-Lancet reference diet to a higher score could reduce food-associated GHG and LU levels by 50% and 62%, respectively.Interpretation: Our results support shifts in diets that
Laine JE, Bodinier B, Robinson O, et al., 2020, Prenatal exposure to multiple air pollutants, mediating molecular mechanisms, and shifts in birthweight., Environmental Science and Technology (Washington), Vol: 54, Pages: 14502-14513, ISSN: 0013-936X
Mechanisms underlying adverse birth and later in life health effects from exposure to air pollution during the prenatal period have not been not fully elucidated, especially in the context of mixtures. We assessed the effects of prenatal exposure to mixtures of air pollutants of particulate matter (PM), PM2.5, PM10, nitrogen oxides, NO2, NO x , ultrafine particles (UFP), and oxidative potential (OP) of PM2.5 on infant birthweight in four European birth cohorts and the mechanistic underpinnings through cross-omics of metabolites and inflammatory proteins. The association between mixtures of air pollutants and birthweight z-scores (standardized for gestational age) was assessed for three different mixture models, using Bayesian machine kernel regression (BKMR). We determined the direct effect for PM2.5, PM10, NO2, and mediation by cross-omic signatures (identified using sparse partial least-squares regression) using causal mediation BKMR models. There was a negative association with birthweight z-scores and exposure to mixtures of air pollutants, where up to -0.21 or approximately a 96 g decrease in birthweight, comparing the 75th percentile to the median level of exposure to the air pollutant mixture could occur. Shifts in birthweight z-scores from prenatal exposure to PM2.5, PM10, and NO2 were mediated by molecular mechanisms, represented by cross-omics scores. Interleukin-17 and epidermal growth factor were identified as important inflammatory responses underlyingair pollution-associated shifts in birthweight. Our results signify that by identifying mechanisms through which mixtures of air pollutants operate, the causality of air pollution-associated shifts in birthweight is better supported, substantiating the need for reducing exposure in vulnerable populations.
Mancini FR, Laine JE, Tarallo S, et al., 2020, microRNA expression profiles and personal monitoring of exposure to particulate matter, Environmental Pollution, Vol: 263, ISSN: 0269-7491
An increasing number of findings from epidemiological studies support associations between exposure to air pollution and the onset of several diseases, including pulmonary, cardiovascular and neurodegenerative diseases, and malignancies. However, intermediate, and potentially mediating, biological mechanisms associated with exposure to air pollutants are largely unknown. Previous studies on the human exposome have shown that the expression of certain circulating microRNAs (miRNAs), regulators of gene expression, are altered upon exposure to traffic-related air pollutants. In the present study, we investigated the relationship between particulate matter (PM) smaller than 2.5 μm (PM2.5), PM2.5 absorbance (as a proxy of black carbon and soot), and ultrafine-particles (UFP, smaller than 0.1 μm), measured in healthy volunteers by 24 h personal monitoring (PEM) sessions and global expression levels of peripheral blood miRNAs. The PEM sessions were conducted in four European countries, namely Switzerland (Basel), United Kingdom (Norwich), Italy (Turin), and The Netherlands (Utrecht). miRNAs expression levels were analysed using microarray technology on blood samples from 143 participants. Seven miRNAs, hsa-miR-24-3p, hsa-miR-4454, hsa-miR-4763-3p, hsa-miR-425-5p, hsa-let-7d-5p, hsa-miR-502-5p, and hsa-miR-505-3p were significantly (FDR corrected) expressed in association with PM2.5 personal exposure, while no significant association was found between miRNA expression and the other pollutants. The results obtained from this investigation suggest that personal exposure to PM2.5 is associated with miRNA expression levels, showing the potential for these circulating miRNAs as novel biomarkers for air pollution health risk assessment.
Laine J, Baltar VT, Stringini S, et al., 2020, Reducing socioeconomic inequalities in all-cause mortality: a counterfactual mediation approach, International Journal of Epidemiology, Vol: 49, Pages: 497-510, ISSN: 0300-5771
Background: Socioeconomicinequalities inmortality arewell established, yet the contribution of intermediate risk factors that may underlie these relationships remains unclear.We evaluated the role of multiple modifiable intermediate risk factors underlyingsocioeconomicassociated-mortality and quantifiedthe potentialimpact of reducing early all-cause mortality by hypothetically altering socioeconomic risk factors. Methods: Data were fromsevencohort studies participating in the LIFEPATH consortium (total n=179,090). Using bothsocioeconomic position (SEP) (based on occupation) and education, we estimated thenaturaldirect effect on all-cause mortality, and thenatural indirect effect via the joint mediatingrole of smoking, alcohol intake, dietary patterns, physical activity, body mass index,hypertension, diabetes, and coronary artery disease.Hazard ratios(HR)were estimated, using counterfactual natural effect modelsunder different hypothetical actions of either lower or higher SEP or education. Results: Lower SEP and educationwereassociated with anincreaseinall-cause mortalitywithin an average follow up time of 17.5 years.Mortality wasreducedviamodelled hypothetical actions of increasing SEP oreducation. Through higher educationtheHR was0.85(95% confidence interval (CI) 0.84, 0.86) for women and 0.71(95% CI 0.70, 0.74)for men,compared to lower education. In addition, 34% and 38% of the effect was jointlymediatedfor womenand men, respectively. The benefits from alteringSEP were slightly more modest.Conclusions: Theseobservational findings supportpoliciesto reducemortalityboththrough improving socioeconomic circumstances and increasing education,andby altering intermediaries, such as lifestyle behaviours and morbidities.
Laine JE, Baltar VT, Stringhini S, et al., 2020, Reducing socio-economic inequalities in all-cause mortality: a counterfactual mediation approach (vol 49, pg 497, 2020), INTERNATIONAL JOURNAL OF EPIDEMIOLOGY, Vol: 49, Pages: 707-707, ISSN: 0300-5771
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Laine JE, Robinson O, 2018, Framing Fetal and Early Life Exposome within Epidemiology, Unraveling the Exposome: A Practical View, Editors: Dagnino, Macherone, Publisher: Springer
Laine J, Fry RC, 2018, Maternal one carbon metabolism and arsenic methylation in a pregnancy cohort in Mexico, Journal of Exposure Science and Environmental Epidemiology, ISSN: 1559-0631
Laine JE, Bailey KA, Olshan AF, et al., 2017, Neonatal Metabolomic Profiles Related to Prenatal Arsenic Exposure, Environmental Science and Technology, Vol: 51, Pages: 625-633, ISSN: 0013-936X
Prenatal inorganic arsenic (iAs) exposure is associated with health effects evident at birth and later in life. An understanding of the relationship between prenatal iAs exposure and alterations in the neonatal metabolome could reveal critical molecular modifications, potentially underpinning disease etiologies. In this study, nuclear magnetic resonance (NMR) spectroscopy-based metabolomic analysis was used to identify metabolites in neonate cord serum associated with prenatal iAs exposure in participants from the Biomarkers of Exposure to ARsenic (BEAR) pregnancy cohort, in Gómez Palacio, Mexico. Through multivariable linear regression, ten cord serum metabolites were identified as significantly associated with total urinary iAs and/or iAs metabolites, measured as %iAs, %monomethylated arsenicals (MMAs), and % dimethylated arsenicals (DMAs). A total of 17 metabolites were identified as significantly associated with total iAs and/or iAs metabolites in cord serum. These metabolites are indicative of changes in important biochemical pathways such as vitamin metabolism, the citric acid (TCA) cycle, and amino acid metabolism. These data highlight that maternal biotransformation of iAs and neonatal levels of iAs and its metabolites are associated with differences in neonate cord metabolomic profiles. The results demonstrate the potential utility of metabolites as biomarkers/indicators of in utero environmental exposure.
Laine JE, Fry RC, 2016, A Systems Toxicology-based Approach Reveals Biological Pathways Dysregulated by Prenatal Arsenic Exposure., Annals of Global Health, Vol: 82, Pages: 189-196, ISSN: 2214-9996
BackgroundPrenatal exposure to inorganic arsenic (iAs) is associated with dysregulated fetal gene and protein expression. Potential biological mechanisms that underlie these changes include, but are not limited to, changes to the epigenome.ObjectiveThe aim of the present study was to identify whether the expression of key genes, proteins, or both and their associated biological pathways are perturbed by compiling datasets from studies on prenatal arsenic exposure.MethodsWe compiled datasets from 12 studies that analyzed the relationship between prenatal iAs exposure and changes to the fetal epigenome (5-methyl cytosine), transcriptome (mRNA expression), and/or proteome (protein expression).FindingsAcross the 12 studies, a set of 845 unique genes was identified and found to enrich for their role in biological pathways, including the peroxisome proliferator-activated receptor, nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, and the glucocorticoid receptor. Tumor necrosis factor was identified as a putative cellular regulator underlying most (n = 277) of the identified iAs-associated gene or protein expression changes.ConclusionsThe identification of the common set of genes across numerous human cohorts suggests a conserved biological response to prenatal arsenic exposure. The genes/proteins and their associated pathways may be useful in future mechanistic investigations of iAs associated diseases.
Laine JE, Ray P, Bodnar W, et al., 2015, Placental Cadmium Levels Are Associated with Increased Preeclampsia Risk, PLoS ONE, Vol: 10, ISSN: 1932-6203
Environmental exposure to heavy metals is a potentially modifiable risk factor for preeclampsia (PE). Toxicologically, there are known interactions between the toxic metal cadmium (Cd) and essential metals such as selenium (Se) and zinc (Zn), as these metals can protect against the toxicity of Cd. As they relate to preeclampsia, the interaction between Cd and these essential metals is unknown. The aims of the present study were to measure placental levels of Cd, Se, and Zn in a cohort of 172 pregnant women from across the southeast US and to examine associations of metals levels with the odds of PE in a nested case-control design. Logistic regressions were performed to assess odds ratios (OR) for PE with exposure to Cd controlling for confounders, as well as interactive models with Se or Zn. The mean placental Cd level was 3.6 ng/g, ranging from 0.52 to 14.5 ng/g. There was an increased odds ratio for PE in relationship to placental levels of Cd (OR = 1.5; 95% CI: 1.1–2.2). The Cd-associated OR for PE increased when analyzed in relationship to lower placental Se levels (OR = 2.0; 95% CI: 1.1–3.5) and decreased with higher placental Se levels (OR = 0.98; 95% CI: 0.5–1.9). Similarly, under conditions of lower placental Zn, the Cd-associated OR for PE was elevated (OR = 1.8; 95% CI: 0.8–3.9), whereas with higher placental Zn it was reduced (OR = 1.3; 95% CI: 0.8–2.0). Data from this pilot study suggest that essential metals may play an important role in reducing the odds of Cd-associated preeclampsia and that replication in a larger cohort is warranted.
Laine JE, Bailey KA, Rubio-Andrade M, et al., 2015, Maternal Arsenic Exposure, Arsenic Methylation Efficiency, and Birth Outcomes in the Biomarkers of Exposure to ARsenic (BEAR) Pregnancy Cohort in Mexico, Environmental Health Perspectives, Vol: 123, Pages: 186-192, ISSN: 0091-6765
Bailey KA, Laine J, Rager JE, et al., 2014, Prenatal Arsenic Exposure and Shifts in the Newborn Proteome: Interindividual Differences in Tumor Necrosis Factor (TNF)-Responsive Signaling, Toxicological Sciences, Vol: 139, Pages: 328-337, ISSN: 1096-6080
Rager JE, Bailey KA, Smeester L, et al., 2014, Prenatal arsenic exposure and the epigenome: Altered microRNAs associated with innate and adaptive immune signaling in newborn cord blood, Environmental and Molecular Mutagenesis, Vol: 55, Pages: 196-208, ISSN: 0893-6692
<jats:p>The Biomarkers of Exposure to ARsenic (BEAR) pregnancy cohort in Gómez Palacio, Mexico was recently established to better understand the impacts of prenatal exposure to inorganic arsenic (iAs). In this study, we examined a subset (<jats:italic>n</jats:italic> = 40) of newborn cord blood samples for microRNA (miRNA) expression changes associated with <jats:italic>in utero</jats:italic> arsenic exposure. Levels of iAs in maternal drinking water (DW‐iAs) and maternal urine were assessed. Levels of DW‐iAs ranged from below detectable values to 236 µg/L (mean = 51.7 µg/L). Total arsenic in maternal urine (U‐tAs) was defined as the sum of iAs and its monomethylated and dimethylated metabolites (MMAs and DMAs, respectively) and ranged from 6.2 to 319.7 µg/L (mean = 64.5 µg/L). Genome‐wide miRNA expression analysis of cord blood revealed 12 miRNAs with increasing expression associated with U‐tAs. Transcriptional targets of the miRNAs were computationally predicted and subsequently assessed using transcriptional profiling. Pathway analysis demonstrated that the U‐tAs‐associated miRNAs are involved in signaling pathways related to known health outcomes of iAs exposure including cancer and diabetes mellitus. Immune response‐related mRNAs were also identified with decreased expression levels associated with U‐tAs, and predicted to be mediated in part by the arsenic‐responsive miRNAs. Results of this study highlight miRNAs as novel responders to prenatal arsenic exposure that may contribute to associated immune response perturbations. Environ. Mol. Mutagen. 55:196–208, 2014. © 2013 The Authors. Environmental and Molecular Mutagenesis Published by Wiley Periodicals, Inc.</jats:p>
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