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1.
Per- and poly-fluoroalkyl substances (PFAS) and female reproductive outcomes: PFAS elimination, endocrine-mediated effects, and disease.
Rickard, BP, Rizvi, I, Fenton, SE
Toxicology. 2022;:153031
Abstract
Per- and poly-fluoroalkyl substances (PFAS) are widespread environmental contaminants frequently detected in drinking water supplies worldwide that have been linked to a variety of adverse reproductive health outcomes in women. Compared to men, reproductive health effects in women are generally understudied while global trends in female reproduction rates are declining. Many factors may contribute to the observed decline in female reproduction, one of which is environmental contaminant exposure. PFAS have been used in home, food storage, personal care and industrial products for decades. Despite the phase-out of some legacy PFAS due to their environmental persistence and adverse health effects, alternative, short-chain and legacy PFAS mixtures will continue to pollute water and air and adversely influence women's health. Studies have shown that both long- and short-chain PFAS disrupt normal reproductive function in women through altering hormone secretion, menstrual cyclicity, and fertility. Here, we summarize the role of a variety of PFAS and PFAS mixtures in female reproductive tract dysfunction and disease. Since these chemicals may affect reproductive tissues directly or indirectly through endocrine disruption, the role of PFAS in breast, thyroid, and hypothalamic-pituitary-gonadal axis function are also discussed as the interplay between these tissues may be critical in understanding the long-term reproductive health effects of PFAS in women. A major research gap is the need for mechanism of action data - the targets for PFAS in the female reproductive and endocrine systems are not evident, but the effects are many. Given the global decline in female fecundity and the ability of PFAS to negatively impact female reproductive health, further studies are needed to examine effects on endocrine target tissues involved in the onset of reproductive disorders of women.
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Home Dust Allergen Exposure Is Associated with Outcomes among Sensitized Individuals with Chronic Obstructive Pulmonary Disease.
Putcha, N, Woo, H, McCormack, MC, Fawzy, A, Romero, K, Davis, MF, Wise, RA, Diette, GB, Koehler, K, Matsui, EC, et al
American journal of respiratory and critical care medicine. 2022;(4):412-420
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Abstract
Rationale: Environmental exposures have been associated with adverse outcomes in chronic obstructive pulmonary disease (COPD). Approximately one-third of individuals with COPD have allergic sensitization, but it is unknown whether exposure to allergens in the home is associated with outcomes. Objectives: To determine the prevalence and associations of allergen sensitization with exposure to common indoor allergens with symptoms and exacerbation risk in COPD. Methods: Allergen sensitization to five common indoor allergens was assessed in former smokers with COPD. Home settled dust was assessed for presence of corresponding allergens. Sensitization and exposure status was determined and associations evaluated in adjusted models with longitudinal outcomes including symptoms, lung function, and exacerbations. Interactions were assessed between sensitization/exposure status and lung function. Measurements and Main Results: One hundred eighty-three individuals studied were on average 67.3 years of age (SD, 8.22) with average FEV1 of 53.2% (SD, 17.6%). Seventy-seven percent of participants were exposed to at least one tested allergen, and 17% had sensitization with corresponding allergen exposure. After adjustment, sensitization with exposure was associated with lower lung function (β, -8.29; 95% confidence interval [CI], -14.80 to -1.77), higher St. George's Respiratory Questionnaire Total Score (β, 6.71; 95% CI, 0.17 to 13.25), and higher exacerbation risk (odds ratio, 2.31; 95% CI, 1.11 to 4.79). Associations appeared to be more pronounced among individuals with lower lung function. Conclusions: Allergen exposures are common in COPD and associated with adverse outcomes among those with concomitant allergen sensitization. This study establishes allergens as an important home exposure that potentially could be addressed with comprehensive home environmental modification strategies to improve COPD outcomes.
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Environmental risk factors of type 2 diabetes-an exposome approach.
Beulens, JWJ, Pinho, MGM, Abreu, TC, den Braver, NR, Lam, TM, Huss, A, Vlaanderen, J, Sonnenschein, T, Siddiqui, NZ, Yuan, Z, et al
Diabetologia. 2022;(2):263-274
Abstract
Type 2 diabetes is one of the major chronic diseases accounting for a substantial proportion of disease burden in Western countries. The majority of the burden of type 2 diabetes is attributed to environmental risks and modifiable risk factors such as lifestyle. The environment we live in, and changes to it, can thus contribute substantially to the prevention of type 2 diabetes at a population level. The 'exposome' represents the (measurable) totality of environmental, i.e. nongenetic, drivers of health and disease. The external exposome comprises aspects of the built environment, the social environment, the physico-chemical environment and the lifestyle/food environment. The internal exposome comprises measurements at the epigenetic, transcript, proteome, microbiome or metabolome level to study either the exposures directly, the imprints these exposures leave in the biological system, the potential of the body to combat environmental insults and/or the biology itself. In this review, we describe the evidence for environmental risk factors of type 2 diabetes, focusing on both the general external exposome and imprints of this on the internal exposome. Studies provided established associations of air pollution, residential noise and area-level socioeconomic deprivation with an increased risk of type 2 diabetes, while neighbourhood walkability and green space are consistently associated with a reduced risk of type 2 diabetes. There is little or inconsistent evidence on the contribution of the food environment, other aspects of the social environment and outdoor temperature. These environmental factors are thought to affect type 2 diabetes risk mainly through mechanisms incorporating lifestyle factors such as physical activity or diet, the microbiome, inflammation or chronic stress. To further assess causality of these associations, future studies should focus on investigating the longitudinal effects of our environment (and changes to it) in relation to type 2 diabetes risk and whether these associations are explained by these proposed mechanisms.
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Associations between exposure to heavy metals and the risk of chronic kidney disease: a systematic review and meta-analysis.
Jalili, C, Kazemi, M, Cheng, H, Mohammadi, H, Babaei, A, Taheri, E, Moradi, S
Critical reviews in toxicology. 2021;(2):165-182
Abstract
We performed a systematic review and meta-analysis to examine the relationship between heavy metals (HMs) exposure and the risk of chronic kidney disease (CKD). Databases of Web of Science, Embase, MEDLINE, and Scopus were searched through June 2020 to identify studies assessing the relationships between exposure to HMs (i.e. cadmium, lead, arsenic, mercury) and the risk of CKD, evaluated by decreased estimated glomerular filtration rate (eGFR) and/or increased proteinuria risks in adults (≥18 years). Data were pooled by random-effects models and expressed as weighted mean differences and 95% confidence intervals. The risk of bias was assessed by the Newcastle-Ottawa scale (NOS). Twenty-eight eligible articles (n = 107,539 participants) were included. Unlike eGFR risk (p = 0.10), Cadmium exposure was associated with an increased proteinuria risk (OR = 1.35; 95% CI: 1.13, 1.61; p < 0.001; I2 = 79.7%). Lead exposure was associated with decreased eGFR (OR = 1.12; 95%CI: 1.03, 1.22; p = 0.008; I2 = 87.8%) and increased proteinuria (OR = 1.25; 95% CI: 1.04, 1.49; p = 0.02; I2 = 79.6) risks. Further, arsenic exposure was linked to a decreased eGFR risk (OR = 1.55; 95% CI: 1.05, 2.28; p = 0.03; I2 = 89.1%) in contrast to mercury exposure (p = 0.89). Only two studies reported the link between arsenic exposure and proteinuria risk, while no study reported the link between mercury exposure and proteinuria risk. Exposure to cadmium, lead, and arsenic may increase CKD risk in adults, albeit studies were heterogeneous, warranting further investigations. Our observations support the consideration of these associations for preventative, diagnostic, monitoring, and management practices of CKD.
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Environmental Determinants of Type 1 Diabetes: From Association to Proving Causality.
Quinn, LM, Wong, FS, Narendran, P
Frontiers in immunology. 2021;:737964
Abstract
The rising incidence of type 1 diabetes (T1D) cannot be ascribed to genetics alone, and causative environmental triggers and drivers must also be contributing. The prospective TEDDY study has provided the greatest contributions in modern time, by addressing misconceptions and refining the search strategy for the future. This review outlines the evidence to date to support the pathways from association to causality, across all stages of T1D (seroconversion to beta cell failure). We focus on infections and vaccinations; infant growth and childhood obesity; the gut microbiome and the lifestyle factors which cultivate it. Of these, the environmental determinants which have the most supporting evidence are enterovirus infection, rapid weight gain in early life, and the microbiome. We provide an infographic illustrating the key environmental determinants in T1D and their likelihood of effect. The next steps are to investigate these environmental triggers, ideally though gold-standard randomised controlled trials and further prospective studies, to help explore public health prevention strategies.
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Perspective on prenatal polychlorinated biphenyl exposure and the development of the progeny nervous system (Review).
Wang, Y, Hu, C, Fang, T, Jin, Y, Wu, R
International journal of molecular medicine. 2021;(2)
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Abstract
The developmental origins of health and disease concept illustrates that exposure in early life to various factors may affect the offspring's long‑term susceptibility to disease. During development, the nervous system is sensitive and vulnerable to the environmental insults. Polychlorinated biphenyls (PCBs), which are divided into dioxin‑like (DL‑PCBs) and non‑dioxin‑like PCBs (NDL‑PCBs), are synthetic persistent environmental endocrine‑disrupting chemicals. The toxicological mechanisms of DL‑PCBs have been associated with the activation of the aryl hydrocarbon receptor and NDL‑PCBs have been associated with ryanodine receptor‑mediated calcium ion channels, which affect neuronal migration, promote dendritic growth and alter neuronal connectivity. In addition, PCB accumulation in the placenta destroys the fetal placental unit and affects endocrine function, particularly thyroid hormones and the dopaminergic system, leading to neuroendocrine disorders. However, epidemiological investigations have not achieved a consistent result in different study cohorts. The present review summarizes the epidemiological differences and possible mechanisms of the effects of intrauterine PCB exposure on neurological development.
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A clandestine culprit with critical consequences: Benzene and acute myeloid leukemia.
Shallis, RM, Weiss, JJ, Deziel, NC, Gore, SD
Blood reviews. 2021;:100736
Abstract
While most clinicians recognize adult therapy-related leukemias following cytotoxic chemotherapy and radiation, environmental regulatory agencies evaluate exposure to "safe levels" of leukemogenic compounds. Benzene represents the most notorious leukemogenic chemical. Used in the production of ubiquitous items such as plastics, lubricants, rubbers, dyes, and pesticides, benzene may be responsible for the higher risk of acute myeloid leukemia (AML) among automobile, janitorial, construction, and agricultural workers. It is possible that ambient benzene may contribute to many cases of "de novo" AML not arising out of germline predispositions. In this appraisal of the available literature, we evaluate and discuss the association between chronic, low-dose and ambient exposure to environmental benzene and the development of adult AML.
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Air pollution and pre-eclampsia; associations and potential mechanisms.
Bearblock, E, Aiken, CE, Burton, GJ
Placenta. 2021;:188-194
Abstract
INTRODUCTION Air pollution has significant negative health impacts, particularly on the cardiovascular system. The aims of this narrative review were to identify whether there is an association between air pollution and the incidence of pre-eclampsia, and the potential mechanisms by which any effects may be mediated. METHODS We undertook a literature search using Google Scholar, PubMed, the Cochrane Library and NICE Evidence. The primary eligibility criterion was articles correlating exposure to air pollution with incidence of pre-eclampsia. RESULTS Meta-analyses currently show a positive association between pre-eclampsia and exposure to both particulate matter PM2.5 and nitrogen dioxide, but no significant associations with ambient ozone or carbon monoxide exposure. No meta-analysis has been performed for exposure to sulfur dioxide. Variability in terms of quantification of exposure, the exposure period and co-founders among the studies makes comparisons complex. Adverse effects on trophoblast invasion and placental vascularisation, and increases in oxidative stress and anti-angiogenic factors, such as sFlt-1, in response to air pollution provide pathways by which exposure may contribute to the pathophysiology of pre-eclampsia. So far, studies have not discriminated between the early- and late-onset forms of the syndrome. DISCUSSION Future prospective studies using personal air pollution monitors and blood biomarkers of pre-eclampsia would strengthen the associations. Interactions between pollutants are poorly documented, and at present there is minimal informed advice available to women on the need to avoid exposure to air pollutants during pregnancy.
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Air Pollution and Asthma: Mechanisms of Harm and Considerations for Clinical Interventions.
Pfeffer, PE, Mudway, IS, Grigg, J
Chest. 2021;(4):1346-1355
Abstract
There is global concern regarding the harmful impact of polluted air on the respiratory health of patients with asthma. Multiple epidemiologic studies have shown ongoing associations between high levels of air pollution and poor early life lung growth, development of allergic sensitization, development of asthma, airway inflammation, acutely impaired lung function, respiratory tract infections, and asthma exacerbations. However, studies have often yielded inconsistent findings, and not all studies have found significant associations; this may be related to both variations in statistical, measurement, and modeling methodologies between studies as well as differences in the concentrations and composition of air pollution globally. Overall, this variation in findings suggests we still do not fully understand the effects of ambient pollution on the lungs and on the evolution and exacerbation of airway diseases. There is clearly a need to augment epidemiologic studies with experimental studies to clarify the underlying mechanistic basis for the adverse responses reported and to identify the key gaseous and particle-related components within the complex air pollution mixture driving these outcomes. Some progress toward these aims has been made. This article reviews studies providing an improved understanding of causal pathways linking air pollution to asthma development and exacerbation. The article also considers potential strategies to reduce asthma morbidity and mortality through regulation and behavioral/pharmacologic interventions, including a consideration of pollutant avoidance strategies and antioxidant and/or vitamin D supplementation.
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Residential exposure to electromagnetic fields and risk of amyotrophic lateral sclerosis: a dose-response meta-analysis.
Filippini, T, Hatch, EE, Vinceti, M
Scientific reports. 2021;(1):11939
Abstract
Amyotrophic lateral sclerosis (ALS) is neurodegenerative disease characterized by a fatal prognosis and still unknown etiology. Some environmental risk factors have been suggested, including exposure to magnetic fields. Studies have suggested positive associations in occupationally-exposed populations, but the link with residential exposure is still debated as is the shape of such relation. Due to recent availability of advanced biostatistical tools for dose-response meta-analysis, we carried out a systematic review in order to assess the dose-response association between ALS and residential exposure to magnetic fields. We performed an online literature searching through April 30, 2021. Studies were included if they assessed residential exposure to electromagnetic fields, based either on distance from overhead power lines or on magnetic field modelling techniques, and if they reported risk estimates for ALS. We identified six eligible studies, four using distance-based and one modelling-based exposure assessment, and one both methods. Both distance-based and particularly modelling-based exposure estimates appeared to be associated with a decreased ALS risk in the highest exposure category, although estimates were very imprecise (summary RRs 0.87, 95% CI 0.63-1.20, and 0.27, 95% CI 0.05-1.36). Dose-response meta-analysis also showed little association between distance from power lines and ALS, with no evidence of any threshold. Overall, we found scant evidence of a positive association between residential magnetic fields exposure and ALS, although the available data were too limited to conduct a dose-response analysis for the modelled magnetic field estimates or to perform stratified analyses.