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Human physiology, hazards and health risks
Published in Stephen Battersby, Clay's Handbook of Environmental Health, 2023
Revati Phalkey, Naima Bradley, Alec Dobney, Virginia Murray, John O’Hagan, Mutahir Ahmad, Darren Addison, Tracy Gooding, Timothy W Gant, Emma L Marczylo, Caryn L Cox
Importantly for intergenerational transmission of environmentally induced epigenetic effects, miRNA are transferred in the gametes in easily measurable quantities where they control the early stages of gene expression in the zygote. Transfer takes place in both the ovum and the spermatozoa. In terms of looking at the effects of the environment on the composition of miRNA in the gametes, there have been more studies in the male by virtue of the tissue being more accessible. For example, tobacco smoking has been shown to have effects on the composition of miRNA in the spermatozoa [21–22]. These are observational studies and so the consequences of the changed composition of miRNA for the zygote the totipotent cells and resulting embryo are not known. Nevertheless, they provide an insight into a potential mechanism by which environmental exposures in one generation may lead to inheritable adaptations in subsequent generations. Qualitative alteration in miRNAs in gametes have also been associated with other environmental exposures [23–24] and diet-induced obesity [25].
Activities Supporting Work Ability in Workers with Chronic Diseases
Published in Joanna Bugajska, Teresa Makowiec-Dąbrowska, Tomasz Kostka, Individual and Occupational Determinants, 2020
Cardiovascular diseases (CVDs) are the number 1 cause of death globally: more people die annually from CVDs than from any other cause. An estimated 17.9 million people died from CVDs in 2016, representing 31% of all global deaths. Of these deaths, 85% are due to heart attack and stroke. Most CVDs can be prevented by addressing behavioural risk factors such as tobacco use, unhealthy diet and obesity, physical inactivity and alcohol abuse using population-wide strategies (WHO 2017). CVDs manifest by numerous symptoms and complications (including stroke, myocardial infarction, or cardiac insufficiency) which lead to temporary or permanent inability to work. The most frequent morbid entities among the CVDs include coronary heart disease and arterial hypertension. Coronary heart disease usually affects economically active people, more often men aged 40–55 years, and among the older population (>55 years of age), the prevalence of this disease is similar in men and women.
Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Among this sample of middle-aged and older women, roadway proximity was associated with an elevation in the risk of SCD. Even after adjustment for potential confounders and mediators, women who lived within 50 m of a major roadway had a 38% higher hazard (95% CI = 1.04–1.82) of experiencing SCD compared with women living ≥500 m away. The association was linear, and each 100 m closer to a major roadway was associated with a 6% elevation in the HR (95% CI = 1–11). Proximity to a major roadway was also statistically significantly associated with fatal CHD but to a lesser magnitude. These results suggest that traffic exposure, as measured by roadway proximity, may increase the risk of death resulting from CHD and may increase the propensity for fatal ventricular arrhythmias. If the observed relationships are causal, these results suggest that roadway exposures may underlie 17.9%, 11.6%, and 6.8% of SCDs, fatal CHDs, and nonfatal MIs, respectively, in this population. For the end point of SCD, these population-attributable risks are comparable to or greater than the contributions made by smoking, diet, and obesity in this population.568 This study is highly significant for the chemically sensitive. They are pollutant sensitive; their vascular area will be prone to pollutant injury just as Hart's implants even though they may not have SCD, they will be kept chronically ill by the pollutant exposure.
Implications of estrogen receptor alpha (ERa) with the intersection of organophosphate flame retardants and diet-induced obesity in adult mice
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Gwyndolin M. Vail, Sabrina N. Walley, Ali Yasrebi, Angela Maeng, Thomas J. Degroat, Kristie M. Conde, Troy A. Roepke
Previously, Vail et al. (2020) demonstrated that sub-chronic OPFR exposure within adult, wildtype mice elicited sex-dependent alterations in feeding behavior and energy homeostasis. These effects interacted with diet-induced obesity, resulting in exposed males gaining more weight and fat mass only when fed a high-fat diet (HFD). In addition, while in exposed females no marked body weight effects were noted, these animals ate less food and consumed fewer HFD meals per day (Vail et al. 2020). Because ERα regulates central and peripheral control of feeding behavior, and since OPFRs are known to interact with ERα, it was postulated that OPFR-initiated dysregulation of energy homeostasis may be associated with disruption of ERα signaling. To further elucidate the association of ERα with the toxicological effects of OPFRs on ingestive behavior, this study utilized global ERα knockout mouse models fed either a LFD or HFD.
The interactions of diet-induced obesity and organophosphate flame retardant exposure on energy homeostasis in adult male and female mice
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Gwyndolin M. Vail, Sabrina N. Walley, Ali Yasrebi, Angela Maeng, Kristie M. Conde, Troy A. Roepke
In summary, our findings indicated that a mixture of three common OPFR compounds exerted disruptive actions on energy homeostasis that subsequently interact with and potentially exacerbate diet-induced obesity. We observed a multitude of sex-dependent effects on metabolism, energy expenditure, weight-gain, activity, water intake and circulating hormone concentrations. Most notable were OPFR alterations to water intake and behavioral activity. Our findings demonstrate the EDC capacity of OPFR to disrupt energy homeostasis, which increases the risk of metabolic disorders such as diet-induced obesity, diabetes, and metabolic syndrome. Despite the apparent risk, OPFRs still continue to be a leading flame retardant in the United States. This reality calls for the need of continued research, if there are to be regulatory actions taken to limit human OPFR exposure. With the multitude of OPFR endpoints, it may be a while yet before one knows the full scope of OPFR-mediated toxicity. However, it would be interesting to investigate the mechanistic roots of the dysregulated fluid homeostasis noted herein, as well as additional behavioral studies to tease out whether the sedentary behavior of OPFR-treated females is a mood, or motivation effect. Further, while this study focused primarily on peripheral and behavioral outcomes, energy homeostasis is tightly regulated through central processes in the hypothalamus. Thus, it will also be important to investigate potential OPFR actions on neuronal subpopulations that regulate feeding and reward pathways in the brain.
Implications of peroxisome proliferator-activated receptor gamma (PPARY) with the intersection of organophosphate flame retardants and diet-induced obesity in adult mice
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Gwyndolin M. Vail, Sabrina N. Walley, Ali Yasrebi, Angela Maeng, Thomas J. Degroat, Kristie M. Conde, Troy A. Roepke
Generally, our experimentations with brain-specific PPARγKO animals revealed that when fed HFD, the effects of OPFR on increased bodyweight and fat mass and altered feeding behavior reported in WT mice were not present in mice lacking neuronal PPARγ. These data suggested that PPARγ is required for OPFR exposure to impact the effects of diet-induced obesity. Conversely, multiple novel effects of OPFR exposure were reported in female, but not male, PPARγKO mice fed LFD (refer to Table 3). Collectively, the data signify an intriguing direct role of PPARγ in EDC actions of OPFRs in a model of diet-induced obesity, and a simultaneous indirect sensitization of alternative, perhaps compensatory pathways when neuronal PPARγ is absent in non-obese female mice.