Essay on Determining Noise Exposure for Insomnia & Hearing Loss

Introduction

Insomnia is the most widespread health problem resulting from the environment caused by external noise in the surroundings. This has also resulted in hearing loss, especially for older people who are more vulnerable. Community members are forced to shift, move, and twitch between sleep stages as they try to find sleep resulting in restlessness. As a result, the quality of sleep and shift from light to deep sleep stages are affected.

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Method of Determining Increased Exposure

The exposure to environmental hazards at home can be determined by analyzing the incident and injury records. Incident and injury records inspire urgency since it enables determine if additional strategies or better equipment are necessary depending on the level of exposure (Baker, Tata, Kendrick & Orton2016). Increased numbers of injuries and incidences reveal increased levels of exposure to environmental hazards.

Types of Associations Between Environmental Hazards and Health Outcomes

The experiment association factor investigates if the frequency of the outcome is altered by cause and effect association based on preventive actions. Human clinical trials and laboratory experiments can manipulate exposures in a controlled environment compared to studies based on social observational epidemiology. Laboratory animals are sacrificed to examine pathological changes and are exposed in a timed way for measurement while being monitored for disease development. Randomized clinical trials provide room for estimation between exposure and outcome by controlling confounding human studies and bias. The biological gradient association reveals that a nonlinear association or threshold exist for many environmental exposures such as exposure to UV rays and disease. A confounder may be attributed to residual confounding concerning the outcome if it exhibits a biological gradient (Lucas & McMichael). As a result, it becomes difficult to demonstrate quantitative relationships, such as the natural gradient curve. There exists a relationship between environmental hazards and health outcomes, which is biologically plausible. Biological knowledge dictates the biological plausibility of the day, often based on prior beliefs rather than logic or data.

Coherence requires that there should be a fit between cause and effect with the known facts of the natural biology and history of the disease. The coherence association tries to determine if there exists a fit between the biological effects of exposure and temporal patterns of exposure with observed disease patterns. Specificity association outlines that a single outcome is a result of a single exposure such as rubella, which is caused by rubella disease. On the contrary, one to one relationship does not occur more often for some conditions. The causal association is strengthened if the association is limited to a defined class with a specified environmental exposure. Examination of the specificity of an outcome is controlled by causal inference and the study design (Lucas & McMichael). The association between a consequence and a defined genotype is manifested on specific environmental conditions in which susceptibility to genetics is essential. Temporality is vital for the association between environmental hazards and health outcomes; that is, the result must be preceded by exposure. Measurement of the issue does not require an analysis of the exposure.

Strong associations have a higher probability of being causal than weak associations since strong associations are not controlled by residual confounding and possess more credence. For a valid measure of association, comprehensive evaluation measurement and the role of chance and minimization of bias are necessary for robust methodology and study design, which is usually hectic for complex influences on health by the environment. Consistency is essential for confidence if the same outcome is obtained in different situations and populations. Conversely, interaction with a chance or third variable and the use of a different method may cause variance in the investigation of the same phenomenon. Valuable insights are enabled if there exists a lack of consistency in the causes of an outcome, thereby calling for further investigation (Lucas & McMichael). The notion of an analogy that depends on the image to see clear cut analogies may enhance similarities by scientists since the weight of evidence belongs to weak associations. Accurate measurement and quantification of exposure may be difficult for all confounders.

Relationship Between Exposure in the Environment and Degenerative Brain

Polluted air contains a toxic cocktail of gasses, metals, non-organic and organic compounds that cause neurodegeneration that results from chronic exposure of these elements. For instance, lead causes a continuous decline in mental and decreases in memory functions due to long-term accumulative exposure. The formation of protein aggregates is enhanced by the deregulation of antioxidant enzymes, which result in oxidative stress. As a result, the degradation systems are overwhelmed, thereby activating glia, which induces neuroinflammation increasing oxidative stress leading to a self-perpetuating cycle (Bert, Mercader, Pujol, Sunyer & Mortamais, 2018). This causes loss of defined regions in the brain activating signaling pathways that promote the accumulation of toxic materials in neural cells that alter epigenetic or genetic regulation.

Reasons for Higher Vulnerability to Toxins in Children Compared to Adults

Adults have more control over the environment than children since they are aware of the risks available and, therefore, can protect their health by making the right choices, unlike children. Besides, the pattern of exposure varies between children and adults due to behavioral differences. As a result, young children get exposed to dust and chemicals as they crawl on soils and floors, which may be accumulated with chemicals and dirt. Children are also at risk of irreversible damage at the early stages of their development when exposed to environmental toxicants. Their digestive, reproductive, immune, and central nervous systems are still developing. Compared to adults, children drink more water, consume more food, and inhale more air in proportion to their weight since they are continually growing. These differences in water, food, and air disproportionately expose children to toxic chemicals. Children are unable to convert toxic chemicals to their toxic forms due to their immature metabolic pathways. Children cannot remove toxic chemicals since they lack these necessary enzymes required for breaking them down in their bodies, making them more vulnerable (Perlroth & Branco, 2017). Neurodegenerative and cancer diseases caused by poisonous chemicals evolve through multiyear and multistage processes, which may begin during infancy. As a result, children have more time to develop chronic conditions than adults exposed later in their lives.

Policies Needed to Protect Vulnerable Populations from Environmental Hazards

Disposal or other releases should be performed in a way that is safe to the environment is considered as the last resort. Pollution should also be minimized and prevented at the source whenever possible. Also, recycling should be performed in a manner that is safe to environmentally if the pollutants are not preventable. Moreover, the treatment of contaminants that cannot be recycled or prevented should be performed safely for the environment. There should also be a pollution prevention program strategic plan that outlines measures for minimizing the use of natural resources, the use of hazardous materials, and greenhouse gas emissions while enhancing a more sustainable economy. Implementation of greener public purchasing programs should be put into place and ensuring that there exist voluntary environmental measures through bilateral agreements between the community, private firms, and the government (Heacock, Kelly, Asante, Birnbaum, Bergman, Bruné & Kamel, 2016). Furthermore, the government may impose market-based instruments and economic incentives such as trade permits and taxes to encourage environmental policy compliance effectively.

References

Baker, R., Tata, L. J., Kendrick, D., & Orton, E. (2016). Identification of incident poisoning, fracture and burn events using linked primary care, secondary care and mortality data from England: implications for research and surveillance. Injury prevention, 22(1), 59-67.

de Prado Bert, P., Mercader, E. M. H., Pujol, J., Sunyer, J., & Mortamais, M. (2018). The effects of air pollution on the brain: a review of studies interfacing environmental epidemiology and neuroimaging. Current environmental health reports, 5(3), 351-364.

Heacock, M., Kelly, C. B., Asante, K. A., Birnbaum, L. S., Bergman, Å. L., Bruné, M. N., ... & Kamel, M. (2016). E-waste and harm to vulnerable populations: a growing global problem. Environmental health perspectives, 124(5), 550-555.

Lucas, R., & McMichael, A. Association or causation: evaluating links between "environment and disease." https://www.scielosp.org/article/bwho/2005.v83n10/792-795/

Perlroth, N. H., & Branco, C. W. C. (2017). Current knowledge of environmental exposure in children during the sensitive developmental periods. Jornal de pediatria, 93(1), 17-27.