Influence of Air pollution on Central Nervous System –An Overview

Air pollution is a multifaceted environmental toxin capable of assaulting the CNS through diverse pathways. Air pollution is a complex mixture of environmental toxicants that assault the CNS through several cellular and molecular pathways to cause disease. Air pollution effects cross from the periphery to the brain through systemic inflammation, and translocation of nanoparticles to the brain, where both the physical characteristics of the particle itself and the toxic compounds adsorbed on the particle may cause damage. Air pollution has also been associated with diseases of the central nervous system (CNS), including stroke, Alzheimer’s disease, Parkinson’s disease, and neurodevelopmental disorders. Air pollution causes neuroin?ammation, oxidative stress, microglial activation, cerebrovascular dysfunction, and alterations in the blood-brain barrier contribute to CNS pathology. The central nervous system (CNS) is the target organ for the detrimental effects of airborne pollutants. Air pollutants such as gases (e.g., ground-level ozone, carbon monoxide, sulfur oxides, and nitrogen oxides), organic compounds (e.g., polycyclic aromatic hydrocarbons and bacterial endotoxins), and toxic metals (e.g., vanadium, lead, nickel, copper, and manganese) that can be found in outdoor and indoorair affect the CNS. Air pollution is a global problem and has become one of the major issues of public health as well as climate and environmental protection. Heavy traffic causes Air pollution, those effects on CNS damage and that there is a clear link between air pollution and neurological diseases. Understanding of the mediators and mechanisms of CNS injury due to air pollution will help to develop preventive and treatment strategies for the protection of individuals at risk

Neurodevelopment of Amazonian Infants: Antenatal and Postnatal Exposure to Methyl- and Ethylmercury

Neurodevelopment as Gesell development scores (GDSs) in relation to mercury exposure in infants (<6 months of age) of one urban center and two rural villages, respectively, of fisherman and cassiterite miners. Mean total hair-Hg (HHg) concentrations of infants from Itapuã (3.95 ± 1.8 ppm) were statistically (P = 0.0001) different from those of infants from Porto Velho (3.84 ± 5.5 ppm) and Bom Futuro (1.85 ± 0.9 ppm). Differences in vaccine coverage among these populations resulted in significantly higher (P = 0.0001) mean ethylmercury (EtHg) exposure in urban infants (150 μg) than in infants from either village (41.67 μg, Itapuã; 42.39 μg, Bom Futuro). There was an inverse significant (Spearman r = −0.2300; P = 0.0376) correlation between HHg and GDS for infants from Porto Velho, but not for the rural infants from Bom Futuro (Spearman r = 0.1336; P = 0.0862) and Itapuã (Spearman r = 0.1666; P = 0.5182). Logistic regression applied to variables above or below the median GDS showed that EtHg exposure (estimated probability = −0.0157; P = 0.0070) and breastfeeding score (estimated probability = −0.0066; P = 0.0536) score were significantly associated with GDS. Conclusion. In nurslings whose mothers are exposed to different levels of fish-MeHg (HHg), a higher score of neurological development at six months was negatively associated with exposure to additional TCV-EtHg. Results should be interpreted with caution because of unaccounted variables

Concerns for Human Health Relating to Methylmercury (MeHg) Toxicity in Aquatic Environment: A Systematic Literature Review

Mercury poses serious health risks to people, and during the last century, its contamination of the ocean's surface has more than doubled. As a result, authorities and organizations have taken measures to shield people from exposure to this dangerous substance. Mercury pollution mainly comes from many anthropogenic activities, such as burning coal and other industrial processes. In addition to polluting food chains in marine and coastal ecosystems, these operations released mercury into the environment, which subsequently accumulated in fish and was ingested by people. Fish eating from marine, estuarine, and freshwater sources is to blame for more than 90% of MeHg (methylmercury) exposure in the United States and most other regions of the world. This systematic review describes the biotransformation of Hg into MeHg, the entry of MeHg into the aquatic food chain/food web, and the bioaccumulation process of MeHg. This article also describes MeHg toxicity in fish. It focuses on the effects of exposure to MeHg on biochemical, histological, and neurological outcomes in humans, as evident from various epidemiological sources

Biodynamic Interfaces Are Essential for Human-Environment Interactions.

AbstractThe environment impacts human health in profound ways, yet few theories define the form of the relationship between human physiology and the environment. It is conjectured that such complex systems cannot interact directly, but rather their interaction requires the formation of an intermediary "interface." This position contrasts with current epidemiological constructs of causation, which implicitly assume that two complex systems transfer information directly while remaining separate entities. Further, it is contended that dynamic, process‐based interfaces incorporate components from all the interacting systems but exhibit operational independence. This property has many consequences, the foremost being that characteristics of the interface cannot be fully resolved by only studying the systems involved in the interaction. The interface itself must be the subject of inquiry. Without refocusing the attention on biodynamic interfaces, how the environment impacts health cannot be discerned. Also see the video abstract here https://youtu.be/XeyjeZeyo4o

Disruption Response Support For Inland Waterway Transportation

Motivated by the critical role of the inland waterways in the United States\u27 transportation system, this dissertation research focuses on pre- and post- disruption response support when the inland waterway navigation system is disrupted by a natural or manmade event. Following a comprehensive literature review, four research contributions are achieved. The first research contribution formulates and solves a cargo prioritization and terminal allocation problem (CPTAP) that minimizes total value loss of the disrupted barge cargoes on the inland waterway transportation system. It is tailored for maritime transportation stakeholders whose disaster response plans seek to mitigate negative economic and societal impacts. A genetic algorithm (GA)-based heuristic is developed and tested to solve realistically-sized instances of CPTAP. The second research contribution develops and examines a tabu search (TS) heuristic as an improved solution approach to CPTAP. Different from GA\u27s population search approach, the TS heuristic uses the local search to find improved solutions to CPTAP in less computation time. The third research contribution assesses cargo value decreasing rates (CVDRs) through a Value-focused Thinking based methodology. The CVDR is a vital parameter to the general cargo prioritization modeling as well as specifically for the CPTAP model for inland waterways developed here. The fourth research contribution develops a multi-attribute decision model based on the Analytic Hierarchy Process that integrates tangible and intangible factors in prioritizing cargo after an inland waterway disruption. This contribution allows for consideration of subjective, qualitative attributes in addition to the pure quantitative CPTAP approach explored in the first two research contributions

Rumores de uma primavera silenciosa: uma revisão das evidências científicas sobre a associação entre exposição ocupacional e ambiental a pesticidas e distúrbios endócrinos

Occupational exposure to some pesticides, and particularly DBCP and chlordecone, may adversely affect male fertility. However, apart from the therapeutic use of diethylstilbestrol, the threat to human reproduction posed by "endocrine disrupting" environmental contaminants has not been supported by epidemiological evidence thus far. As it concerns other endocrine effects described in experimental animals, only thyroid inhibition following occupational exposure to amitrole and mancozeb has been confirmed in humans. Cancer of the breast, endometrium, ovary, prostate, testis, and thyroid are hormone-dependent, which fostered research on the potential risk associated with occupational and environmental exposure to the so-called endocrine-disrupting pesticides. The most recent studies have ruled out the hypothesis of DDT derivatives as responsible for excess risks of cancer of the reproductive organs. Still, we cannot exclude a role for high level exposure to o,p'-DDE, particularly in post-menopausal ER+ breast cancer. On the other hand, other organochlorine pesticides and triazine herbicides require further investigation for a possible etiologic role in some hormone-dependent cancers

Subclinical neurotoxicity of mercury: a behavioural, molecular mechanisms and therapeutic perspective

ABSTRACT This paper summarizes some recent research works performed during the last 20 years on the molecular mechanisms associated with mercury (Hg) effects on cognitive function. The study will provide a behavioral, molecular and therapeutic perspective from studies that suggest that mercury is neurotoxic metal with diverse effects on cellular functions in the brain. Mercury (Hg), and the organometallic compounds formed from it, are among the most toxic of substances to the global environment. Mercury exists in a wide variety of physical and chemical states, each of which has unique characteristics of target organ toxicity. Ultimately exposure to it can lead to neural destruction and degenerative disease, mercury vapor exposure from dental amalgam has been demonstrated to exceed the sum of all other exposure sources. Although mercury toxic potency is now widely known, its existence in the environment and in several man-made applications makes human exposure inevitable. There are many mechanisms that cause cellular destruction, that is why studies on different adverse mechanisms, and new methodological developments broaden the knowledge of the toxicity of this metal. For experiments on mercuric mercury, methyl mercury toxicity, several methods and cultures of different neural cell types were used. The study will also describe a non-pharmacological therapeutic approach, environmental enrichment, as promising strategy to reverse Hg effects on cognitive function