PubMed Health⌕ Search

PubMed · 12117750

Spine ergonomics.

Abstract

Occupational low back pain (LBP) is an immense burden for both industry and medicine. Ergonomic and personal risk factors result in LBP, but psychosocial factors can influence LBP disability. Epidemiologic studies clearly indicate the role of mechanical loads on the etiology of occupational LBP. Occupational exposures such as lifting, particularly in awkward postures; heavy lifting; or repetitive lifting are related to LBP. Fixed postures and prolonged seating are also risk factors. LBP is found in both sedentary occupations and in drivers as well as those involved in manual materials handling. Any prolonged posture will lead to static loading of the soft tissues and cause discomfort. Standing and sitting have specific advantages and disadvantages for mobility, exertion of force, energy consumption, circulatory demands, coordination, and motion control. The seated posture leads to inactivity causing an accumulation of metabolites, accelerating disk degeneration and leading to disk herniation. Driver's postures can also lead to musculoskeletal problems. Workers in a driving environment are often subjected to postural stress leading to back, neck, and upper extremity pain. This exacerbates the problems due to the vibration. Prevention is by far the treatment of choice. Improved muscle function can be preventative. Poor coordination and motor control systems are as important as endurance and strength. Fixed postures should be avoided. Seats offering good lumbar support should be used in the office. A suspension seat should be used in vehicles whenever possible. Heavy and awkward lifting should be avoided and lifting aids should be made available. Workers should report LBP as early as possible and seek medical advice if they think occupational exposure is harming them. The combined effects of the medical community, labor, and management are required to cause some impact on this problem.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Malcolm H Pope, Kheng Lim Goh, Marianne L Magnusson. 2002-03-22. Spine ergonomics.. https://doi.org/10.1146/annurev.bioeng.4.092101.122107

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Assessing the comorbidity between asthma and depression through polygenic risk scoring and time-to-event models.

BACKGROUND: Patients with asthma have an increased risk of developing depression, affecting their quality of life. To date, the processes contributing to this comorbidity remain unclear. METHODS: We integrated two large genome-wide association studies (88,486 patients with asthma and 447,859 controls; 412,024 patients with depression and 1,587,577 controls) with cross-sectional and longitudinal information available from the All of Us Research Program (N = 87,167) through polygenic risk scoring (PRS), Cox proportional-hazards models, one-sample Mendelian randomization (MR), and gene-set and drug-repurposing analyses. RESULTS: We observed that depression PRS was associated with increased asthma risk (hazard ratio, HR = 1.13, 95% CI = 1.09-1.17), also when accounting for comorbidity status (HR = 1.08, 95% CI = 1.04-1.12). Conversely, the effect of asthma PRS was null after accounting for comorbidity status. One-sample MR analysis showed an effect of depression genetic liability on asthma, ranging from beta = 0.36 ± 0.03 when considering a linear relationship to beta = 3.21 ± 0.31 when considering possible nonlinear relationships. Conversely, the effect of asthma genetic risk on depression was null after accounting for potential confounders. The gene-set analyses showed that asthma and depression polygenic risks share biological processes, molecular functions, and cellular components related to the immune system and the lung-brain axis. CONCLUSIONS: Genetic predisposition contributes to asthma-depression comorbidity through direct effects and shared pathogenic processes. These findings highlight the potential to develop targeted interventions to prevent and treat the co-occurrence of respiratory and neuropsychiatric disorders.

Comorbidity↗