Relationships and Mechanisms Between Occupational Risk Factors and Distal Upper Extremity Disorders

Abstract

Objective

The relationships between workplace risk factors and upper extremity injuries from epidemiological and laboratory studies were examined.

Background

Epidemiological studies are associated with several limitations, affecting the strength of association between risk factors and the development of injuries.

Method

In this narrative review, we identified epidemiological and laboratory studies (published primarily since 1997) investigating exposure to workplace risk factors (force, repetition, posture, vibration) and risk of hand/wrist tendon–related disorders, epicondylitis, and carpal tunnel syndrome (CTS).

Results

Forceful exertions are strongly associated with hand/wrist tendon–related disorders, epicondylitis, and CTS. Dose–response relationships were found for epicondylitis (repetition) and CTS (posture). Interactions demonstrate multiplicative effects of risk factors for injury risk. Laboratory studies display clear associations between task demands and biomechanical measures linked to mechanisms for upper extremity injuries with animal models providing further evidence of a dose–response between risk factors and injury.

Conclusion

Forceful, repetitive work requiring non-neutral postures are associated with increasing risk of hand/wrist tendon–related disorders, epicondylitis, and CTS as evidenced by epidemiology studies and laboratory-based investigations of humans and animals.

Application

Understanding the relationship between exposure levels of workplace risk factors and upper extremity disorders can improve injury prevention and rehabilitation strategies.

Keywords

epidemiology biomechanics upper extremity musculoskeletal system injury

Introduction

Perhaps the biggest question asked of ergonomists is, “How much is too much?” This is a difficult question to answer for disorders of the upper extremity that may take weeks, months, or even years to develop. Evidence is accrued through workplace epidemiology studies and more basic laboratory studies. Workplace epidemiology studies provide information such as the injury risk for workers being exposed to features, or risk factors, of the workplace relative to workers not being exposed or exposed to lower levels of those features. Relative risk (RR), odds ratios (ORs), and hazard ratios (HRs) are presented as epidemiological evidence for/against workplace risk factors and injury risk. Although they differ technically, they each are interpreted as the degree to which exposure to a certain workplace risk factor(s) relate to the risk of injury. Epidemiological studies provide RR, but it can be challenging to determine dose–response relationships due to several limitations. Heterogeneity in injury diagnostic criteria and quantifying workplace exposures across studies, low numbers of injuries, and potential confounders (e.g., worker self-selection bias, controlling for non-workplace exposures) are among the factors that make it challenging to robustly quantify the strength of the relationship between exposures and work-related injuries. Laboratory studies are much less representative of the workplace but aim to identify potential injury mechanisms under a strict set of controlled parameters. Consequently, laboratory experiments help inform the strength and temporal relationship between an isolated exposure and outcome. By examining laboratory studies in the context of their evaluation of risk factors determined from epidemiological studies, we aim to shed light on the dose–response relationships in tendon-related disorders of the hand and wrist (including tendinitis, tenosynovitis, and peritendinitis), epicondylitis, and carpal tunnel syndrome (CTS; median neuropathy at the wrist). This review is presented in three sections, each providing epidemiological and laboratory evidence from the literature in a narrative review.

An extensive review of the literature was conducted to find relevant quantitative epidemiological (observational) and laboratory-based (experimental) studies relating physical workplace exposures to distal upper extremity musculoskeletal disorders (MSDs). Studies published post-1997 were the focus to update the current state of evidence from the landmark reviews from the National Institute for Occupational Safety and Health (NIOSH) by Bernard (1997) and the National Research Council and the Institute of Medicine (2001); however, certain “hallmark” papers prior to 1997 were referenced to provide context. The search used PubMed and Google Scholar. Reference lists and the “cited by” function in Google Scholar were used to capture recent studies. Only articles published in English were included. The primary inclusion/exclusion criteria were guided by the Mixed Methods Appraisal Tool (Hong, Gonzalez-Reyes, & Pluye, 2018) for the epidemiology studies as follows:

Occupational task demands appropriately quantified physical workplace exposure. The main task demands of interest were repetition, force, posture, and vibration. Due to measurement heterogeneity of task demands, studies were included as long as the authors could evaluate independent task demands and multiplicative effects between exposures. As the primary goal of the review was to evaluate the dose–response relationship between physical exposures and MSDs, studies were only included if they explicitly quantified levels of exposure (e.g., high vs. low repetition) rather than dichotomous yes/no criteria (e.g., repetitive vs. not repetitive). Studies objectively quantifying physical exposures were valued higher than self-reported workplace demands, although both were included.

Prevalence and incidence of distal upper extremity MSDs were objectively based on specified, cited criteria involving a combination of medical history, physical examination, and diagnostic testing. Studies evaluating general pain symptoms or grouping multiple MSDs together were not included as it did not allow evaluation of the relationship of exposures to specific health outcomes. The three MSD categories of interest were (a) hand/wrist tendon–related injuries, (b) epicondylitis, and (c) carpal tunnel syndrome.

Participant characteristics were well defined, including the number of workers (eligible, included), task description, workplace settings, and dropout rate (longitudinal studies). These details allowed assessment of the representation of sampled workers to the target population. Studies accounting for confounders by adjusting statistical models using covariates (e.g., age, gender) were valued higher. Study limitations including small sample sizes, few number of incident cases, and survivor or self-selection bias are noted throughout the review.

Similar inclusion/exclusion criteria were used for laboratory-based studies; however, outcome measures were expanded to include biomechanical measures that are hypothesized to contribute to the injury mechanism and progression for the MSDs of interest.

Tendon-Related MSDs of the Hand and Wrist

Hand/wrist tendon–related MSDs include injuries affecting the tendon (tendinitis), tendon sheath/synovium (tenosynovitis), and paratenon (peritendinitis). De Quervain’s disease is a unique case of stenosing tenosynovitis that afflicts the abductor pollicis longus (APL) and extensor pollicis brevis (EPB) muscles. Common signs and symptoms of tendon-related MSDs include pain/tenderness on palpation and resisted exertion, swelling, and crepitus. It is debated whether inflammatory signs are present among these tendon-related MSDs (Schuind, Ventura, & Pasteels, 1990; Scott, Backman, & Speed, 2015; Xu & Murrell, 2008), prompting many investigators to use the global terms tendinopathy and/or tendinosis (Piligian et al., 2000). Most cases of tendinitis are actually considered peritendinitis, with pain localized relatively proximally at the forearm (muscle-tendon junction) (Ranney, 1997; Viikari-Juntura, 1984). Tendon-related MSDs are diagnosed through physical examination, but are often lumped together. We will use the term hand/wrist tendon–related MSDs to collectively refer to the various injuries. However, distinctions between disorders will be made if distinguished by epidemiology studies or to highlight important injury mechanistic differences. This section evaluates seven epidemiological evidence and a number of lab-based experiments quantifying the relationship and mechanisms for hand/wrist tendon–related MSDs across varying levels of workplace exposures for force, repetition, posture, as well as interactions between risk factors. Table 1 summarizes the data from the reviewed and included epidemiology studies.

Table 1

Summary of Workplace Epidemiological Evidence on Hand/Wrist Tendon–Related MSDs

Study	Design	Cohort	MSDs	Results
Kuorinka and Koskinen (1979)	Cross-sectional	93 factory workers: scissors making 96.8% female Age: 32.3 ± 11.7 years	Based on physical examination: muscle-tendon syndrome	Repetition: Cycle time (s) Short-cycle (2.0–9.5 s) vs. long-cycle tasks (7.3–26.1 s): OR = 1.58 [0.61, 4.09] Note: OR [95% CI] were calculated manually based on results.
Armstrong, Fine, Goldstein, Lifshitz, and Silverstein (1987)	Cross-sectional	652 industrial workers from different worksites: electronics, sewing, appliance, bearing fabrication, bearing assembly, investment molding Age: ~40 ± 10 years	Based on physical examination: De Quervain’s Trigger finger Tendinitis Tenosynovitis	Force: Average hand force requirements High (>40 N) vs. low (<10 N): OR = 6.1 Repetition: Cycle time (s) and % cycle performing same motion High vs. low: OR = 3.3 (Cut-off 30 s cycle time and/or 50% cycle = same motion) Interaction (Force × Repetition): High force/repetition vs. low force/repetition: OR = 29.4* Note: OR adjusted for worksite.
Latko et al. (1999)	Cross-sectional	352 manufacturing workers 41.5% female Age: 41.3 ± 10.5 years	Based upon physical examination: Distal upper extremity tendinitis Note: No subjects exhibited classic signs of tendinitis (redness, swelling)	Repetition: Measured on a 0- to 10-visual analog scale (VAS) Medium vs. low (ΔVAS = 3.0): OR = 1.87 [1.13, 3.10] High vs. low (ΔVAS = 5.6): OR = 3.23 [1.27, 8.26] High vs. medium (ΔVAS = 2.6): OR = 1.72 [1.11, 2.66]
Thomsen et al. (2007)	Cross-sectional; prospective (3 years)	3,123 industrial workers 813 (26%) = reference group (“non-repetitive work”) 58.4% female Age: 38.6 ± 10.7 years	Diagnoses based on pain and tenderness on palpation: Definite extensor tendinitis Possible extensor tendinitis Notes: Few cases of definite extensor tendinitis were observed; not included in the analysis	Force: Self-assessed on 5-point scale Continuous: OR = 1.9 [1.1, 3.3]; OR = 2.9 [1.3, 6.8] Low (0–1) vs. reference: OR = 1.3 [0.6, 2.9]; OR = 0.6 [0.2, 1.8] High (>1) vs. reference: OR = 1.7 [0.7, 4.1]; OR = 0.5 [0.1, 1.8] Repetition: Number of repetitions per minute Continuous: OR = 1.6 [0.8, 3.2]; OR = 1.4 [0.5, 4.0] Low (1–12) vs. reference: OR = 1.3 [0.6, 2.9]; OR = 0.6 [0.2, 1.7] High (>12) vs. reference: OR = 1.6 [0.6, 4.3]; OR = 1.1 [0.2, 4.2] Posture: % time out of neutral wrist Continuous: OR = 1.4 [1.0, 2.0]; OR = 1.0 [0.6, 1.6] Low (1–21.7) vs. reference: OR = 1.4 [0.6, 3.1]; OR = 0.6 [0.2, 1.7] High (>21.7) vs. reference: OR = 1.8 [0.8, 3.8]; OR = 0.5 [0.1; 1.6]
				Notes: OR adjusted for potential confounders (age, gender, physical activity, BMI, history of disease, mental health). OR [95% CI] for each level are for prevalence and incidence, respectively. Significant participant dropout, especially at high exposure levels. Cut-offs for exposures are for prevalence analysis, similar thresholds used for incidence.
Petit Le Manac’h et al. (2011)	Cross-sectional	3,710 white- and blue-collar workers42% femaleAge: 38.7 ± 10.3 years	Based on physical exam: De Quervain’s	Force: Rating perceived exertion on the Borg Scale ≥13Yes vs. no: OR = 2.7 [1.4, 5.2]Repetition: High repetitiveness ≥4 hr/dayYes vs. no: OR = 2.4 [1.3, 4.4]^† Posture:Holding tools in pinch grip ≥4 hr/dayYes vs. no: OR = 2.0 [0.9, 4.5]Precise finger movements ≥2 hr/dayYes vs. no: OR = 2.8 [1.5, 5.4]Pressing with base of palm ≥2 hr/dayYes vs. no: OR = 3.2 [1.4, 7.4]Keying and computer work ≥4 hr/dayYes vs. no: OR = 0.4 [0.2, 0.9]Interaction (Repetition × Posture):Repeated/sustained movement turning driving screw ≥2 hr/dayYes vs. no: OR = 5.9 [3.0, 11.5]^† Repeated/sustained wrist bending ≥2 hr/dayYes vs. no: OR = 3.8 [2.1, 7.1]^† Note: OR adjusted for gender. Risk factors (repeated/sustained movement turning driving screw and wrist bending) included in the final multivariate predictive model are denoted with a †.
Harris, Eisen, Goldberg, Krause, and Rempel (2011) and Harris-Adamson, You, Eisen, Goldberg, and Rempel (2014)	Prospective (28 months)	413 industrial workers36.6% femaleAge: 212 workers <40 years and 201 workers ≥40 years	Based on physical examination: wrist flexor and extensor tendinosis, including trigger finger	Force (Harris et al. 2011):Tool weight (kg): low (≤0.6), medium (0.6–0.91), high (>0.91)Medium vs. low: HR = 0.06 [0.01, 0.28]High vs. low: HR = 0.47 [0.18, 1.21]Normalized peak force: low (≤1.49), medium (1.49–4.92), high (>4.92)Medium vs. low: HR = 0.82 [0.32, 2.08]High vs. low: HR = 4.68 [1.71, 12.77]Repetition (Harris et al. 2011):Efforts per minute—observer-rated: low (≤13.33), high (>13.33)High vs. low: HR = 0.05 [0.01, 0.40]Speed of work: low (≤2.67), medium (2.67–3.06), high (>3.06)Medium vs. low: HR = 0.22 [0.05, 1.00]High vs. low: HR = 0.45 [0.18, 1.14]Repetitions per minute in all grips—video analysis: low (≤38.88), medium (38.88–47.24), high (>47.24)Medium vs. low: HR = 1.40 [0.57, 3.43]High vs. low: HR = 0.93 [0.36, 2.41]
			De Quervain’sIntersection syndromeNote: There were very few diagnosed cases.	Posture (Harris et al. 2011):0–5 point scale: low (≤2), medium (2–3), high (>3)Medium vs. low: HR = 3.04 [1.09, 8.48]High vs. low: HR = 0.95 [0.36, 2.50]Posture—a priori analysis (Harris-Adamson et al. 2014):TWA median wrist extension across all hand postures: low (≤16.6°), medium (16.6°–21.7°), high (>21.7°)Medium vs. low: HR = 1.93 [0.68, 5.49]High vs. low: HR = 1.03 [0.34, 3.13]No significant differences when grouping in heavy pinch grip; reduced HR comparing high vs. low exposure for heavy power.TWA median wrist flexion across all hand postures: low (≤2.8°), medium (2.8°–7.1°), high (>7.1°)Medium vs. low: HR = 0.95 [0.34, 2.67]High vs. low: HR = 2.69 [1.01, 7.21]No differences when grouping in heavy pinch and power grips.Posture—post hoc analysis (Harris-Adamson et al. 2014):TWA % time ≥30° wrist extension: low (≤18.8%), medium (18.8%–30.1%), high (>30.1%)Medium vs. low: HR = 1.90 [0.65, 5.52]High vs. low: HR = 0.86 [0.31, 2.40]Reduced HR when comparing high vs. low exposure in heavy power grip; no differences when grouped by heavy pinchTWA % time in ≥30° wrist flexion: low (≤0.1%), medium (0.1%–0.6%), high (>0.6%)Medium vs. low: HR = 0.24 [0.08, 0.73]High vs. low: HR = 0.65 [0.25, 1.73]No differences when grouped by heavy pinch and power grips.Interaction (Force × Repetition × Posture):Repetitions per minute in heavy pinch or power grip: low (≤4.52), medium (4.52–19.2), high (>19.2)Medium vs. low: HR = 1.40 [0.54, 3.59]High vs. low: HR = 1.29 [0.47, 3.49]Notes: Above results are from univariate analyses. In multivariate analysis, only high exposure of normalized peak force significantly increased risk of tendinosis. TWA calculations based on self-reported time spent for each task. Exposure category thresholds calculated by balancing number of cases in each level.

Note. MSDs = musculoskeletal disorders; OR = odds ratio; CI = confidence Interval; HR = hazard ratio; TWA = time weighted average; BMI = body mass index.*p < 0.001.

Epidemiological Evidence

Force

Epidemiological studies display a consistent dose–response relationship between increasing force levels and risk of hand/wrist tendon–related MSDs (Table 1). Three of the four studies assessing workplace forces exhibit a general pattern of greater force exposures related to increasing prevalence and incidence of tendon-related MSDs (Harris, Eisen, Goldberg, Krause, & Rempel, 2011; Petit Le Manac’h et al., 2011; Thomsen et al., 2007), with Armstrong, Fine, Goldstein, Lifshitz, and Silverstein (1987) reporting no significant effects. Of these studies, Thomsen et al. (2007) provide the clearest evidence for a dose–response relationship. In a cohort of 3,123 industrial workers, increasing force was significantly associated with higher prevalence of possible wrist extensor tendinitis (OR = 1.9); however, only a small number of definite tendinitis cases were observed and hence, not included in the analysis. Force was also a significant predictor of possible tendinitis incidence upon a 3-year follow-up (OR = 2.9), indicating a temporal association between exposure and MSD. Both prevalence and incidence results were adjusted for potential confounders (e.g., age, gender, history of disease), and force remained a significant predictor when repetition and posture factors were included in the model. It should be noted that force was assessed subjectively on a 5-point scale, with null findings when workers were grouped discretely into high and low exposure levels based on the median force compared with “non-repetitive” workers. Similarly, high physical demand (>13 on the Borg scale), assessed subjectively in 3,710 white- and blue-collar workers, was independently associated with de Quervain’s disease (OR = 2.7) (Petit Le Manac’h et al., 2011), but not after adjusting for other workplace exposures. Using direct measurement with force gauges or force matching of pinch/power grips, Harris et al. (2011) grouped 413 manual laborers into three exposure levels (low, medium, high) of task-specific time-weighted normalized peak force. Only high force exposures were significantly associated with wrist tendinosis incidence over a 28-month period relative to low force (HR = 4.68). In addition, high normalized peak pinch and power grip forces remained a significant predictor of injury risk when adjusting for age, gender, and different methods of quantifying force (HR = 3.26). In contrast, self-reported and composite scores incorporating force (e.g., Strain Index, American Conference of Governmental Industrial Hygienists Threshold Limit Value for Hand Activity Level (ACGIH TLV for HAL) did not exhibit significant associations, but the authors cautioned against strong conclusions due to sample size limitations. Estimating hand forces from tool weights and electromyography, Armstrong et al. (1987) found trends toward increased risk of tendinitis/tenosynovitis among workers exposed to high forces (>40 N) compared with low-force jobs (OR = 6.1); however, this relationship was not significant (p values or confidence intervals [CIs] were not reported, precluding assessment about the strength of the relationship).

Repetition

The association between repetition and hand/wrist tendon–related MSDs is inconsistent across epidemiological studies (Table 1). Of the six studies assessing repetition, two found evidence of a dose–response relationship (Latko et al., 1999; Petit Le Manac’h et al., 2011), and four did not (Armstrong et al., 1987; Harris et al., 2011; Kuorinka & Koskinen, 1979; Thomsen et al., 2007). Repetition, based on hand activity level using a 0 to 10 visual analog scale (VAS), exhibited a linear relationship with tendinitis prevalence among 352 manufacturing workers categorized into three exposure groups (Latko et al., 1999). An increase in exposure lead to approximately a twofold increase in risk of tendinitis (low-medium OR = 1.87; medium-high OR = 1.71), with individuals exposed to high levels of repetition three times more likely to exhibit tendinitis symptoms than low repetition workers (low-high OR = 3.23). However, classical signs of tendinitis (swelling/redness) were not found in any cases. Prevalence of tendinitis was three times greater among high- versus low-repetitive jobs assessed by video across seven manufacturing worksites (cutoff: cycle time <30 s; >50% of cycle time performing same motion) (Armstrong et al., 1987). Although not significant, the absence of CIs and p values precludes further assessment of strength of association. Also, grouping workers based on cycle times, Kuorinka and Koskinen (1979) observed no effect of repetition. It should be acknowledged that both short (2.0–9.5 s) and long cycle (7.3–26.1 s) tasks meet the criteria for highly repetitive work based on Armstrong et al. (1987), which may explain the elevated MSD prevalence among both groups (short cycle = 22.9%; long cycle = 15.9%). Petit Le Manac’h et al. (2011) reported an independent association between self-reported highly repetitive work (>4 hr/day) and de Quervain’s disease (OR = 2.4). After adjusting for confounders and workplace exposures, this relationship was not significant (OR = 1.8; p = .09). On the contrary, repetition, quantified by the number of exertions per minute, did not significantly predict baseline prevalence or long-term incidence of tendon-related MSDs (Harris et al., 2011; Thomsen et al., 2007).

Posture

There are conflicting effects of posture on hand/wrist tendon–related MSDs (Table 1). Studies observe patterns of increased risk (Harris et al., 2011; Harris-Adamson, You, Eisen, Goldberg, & Rempel, 2014; Petit Le Manac’h et al., 2011; Thomsen et al., 2007) and no difference (Armstrong et al., 1987; Harris-Adamson et al., 2014; Kuorinka & Koskinen, 1979; Petit Le Manac’h et al., 2011) for workplace injuries due to deviated postures and gripping patterns. The most comprehensive analyses were found in a 28-month longitudinal study assessing wrist flexion/extension postures using video across 413 manufacturing workers (Harris et al., 2011; Harris-Adamson et al., 2014). In their initial analysis, time-weighted average (TWA) wrist postures were classified qualitatively into three exposure levels: low (“very good” or “good” posture), medium (“fair”), and high (“bad” or “very bad”) (Harris et al., 2011). Relative to low exposures, medium (HR = 3.04) but not high (HR = 0.95) exposures were associated with greater tendinosis incidence. In the subsequent paper (Harris-Adamson et al., 2014), TWA median wrist posture was grouped into three levels for wrist extension (low: ≤16.6°; medium: 16.6°–21.7°; high: >21.7°) and wrist flexion (low: ≤2.8°; medium: 2.8°–7.1°; high: >7.1°). Risk of wrist tendinosis increased among tasks with high exposures of wrist flexion (HR = 2.69) relative to low exposures, with no significant differences found across wrist extension. It should be highlighted that there was a low incidence of MSDs, with cut-offs determined by distributing the number of cases equally into tertiles. The 5° difference separating exposure levels approximates error commonly associated with video analysis (noted to be 5° in this study). It was reported that the percent time spent in some posture categories were very small (e.g., high: >0.6% time spent in ≥30° flexion). A similar caveat was reported by Thomsen et al. (2007), noting an unequal representation of non-neutral wrist postures but finding a borderline significant association between percent time spent in non-neutral wrist postures and tendinitis prevalence (OR = 1.4; 95% CI [1.0–2.0]). Kuorinka and Koskinen (1979) and Armstrong et al. (1987) found no significant effects of wrist posture on MSD risk, but results were minimally reported, limiting discussion. Using self-reported questionnaires, Petit Le Manac’h et al. (2011) found significant or trending independent risk factors for de Quervain’s disease for precise finger movements (OR = 2.8), pressing with base of palm (OR = 3.2), and holding pinch grip (OR = 2.0). After controlling for other workplace and individual factors, no postural factors remained significant.

Interactive effects of risk factors

The seminal work by Armstrong, Silverstein, and Fine provided substantial epidemiological evidence supporting the interactive effects of risk factors on workplace MSD prevalence (Armstrong et al., 1987). Using force and repetition thresholds, 652 workers were divided into four exposure groups: low force-low repetition (LOF.LOR), high force-low repetition (HIF.LOR), low force-high repetition (LOF.HIR), and high force-high repetition (HIF.HIR). Relative to the LOF.LOR group, the independent effects of force (HIF.LOR OR = 6.1) and repetition (LOF.HIR OR = 3.3) displayed trends toward increased risk of hand/wrist tendinitis but more importantly, both factors together displayed a significant multiplicative effect on risk (HIF.HIR OR = 29.4) (Armstrong et al., 1987). Similarly, Petit Le Manac’h et al. (2011) observed an interactive effect between repetition and posture. Both repeated/sustained wrist bending (OR = 2.6) and movement turning screw (OR = 3.4) were risk factors for de Quervain’s disease, even after adjustment for other biomechanical exposures. It should be acknowledged that Thomsen et al. (2007) found no significant interactions between force, repetition, and posture on prevalence and incidence of tendinitis; however, these results were not reported.

Lab-Based Experimental Evidence

Tendon frictional work is postulated as a central biomechanical measure in the relationship between workplace risk factors and injury, especially pertaining to tenosynovitis (Moore, Wells, & Ranney, 1991; Tanaka & McGlothlin, 1993). Frictional force is encountered due to shear contact stresses, as well as deformation of the tendons and subsynovial connective tissue (SSCT), a multilayered structure facilitating tendon motion (Filius et al., 2017; Kociolek, Tat, & Keir, 2015). Compared with 11 other biomechanical measures, frictional work was modeled as the most sensitive to changes in workplace exposures (force, repetition, posture) and the best predictor of hand/wrist workplace injuries (Moore et al., 1991). The Biomechanics group at the Mayo Clinic have led the field on quantifying in vivo tendon frictional forces. Measuring friction between the flexors and the finger annular pulleys, it was observed that tendon gliding resistance increased with finger motion and tendon loads (Uchiyama, Amadio, Coert, Berglund, & An, 1997; Uchiyama, Amadio, Ishikawa, & An, 1997; Uchiyama, Coert, Berglund, Amadio, & An, 1995). However, friction-induced damage to the tendon sheath around the annular pulley is often associated with trigger finger. Injuries to the wrist/finger tendons exhibit localized damage at the distal wrist crease, indicating that frictional work and contact forces between the tendons and carpal tunnel structures contribute to the development of tenosynovitis (Armstrong, Castelli, Evans, & Diaz-Perez, 1984). Specific to the carpal tunnel, finger flexor gliding resistance increases with wrist flexion, increased tendon excursion, and faster tendon velocities (Filius et al., 2017; Zhao et al., 2007). Differential motion between the fingers also exhibits greater gliding resistance relative to concurrent finger motion (Tat, Kociolek, & Keir, 2013; Zhao et al., 2007). This is believed to be a consequence of the shared synovium across the finger flexors (Ettema, Zhao, An, & Amadio, 2006; Zhao et al., 2007), suggesting that risk of tendon-related MSDs may be elevated among tasks primarily requiring pinching or single finger press compared with power grips. Similarly, gliding resistance of the APL and EPB tendons in the first dorsal compartment is elevated with deviated wrist postures, especially at end range wrist flexion, and with radial deviation for the EPB (Kutsumi, Amadio, Zhao, Zobitz, & An, 2005), thus having implications for de Quervain’s disease. Simulating low force (20 N), highly repetitive (1 Hz) work by cyclically loading the flexor digitorum superficialis (FDS) tendons in monkeys, frictional forces were found to increase over a 6-hr period even when treated with saline (Smutz, Miller, Eaton, Bloswick, & France, 1994). Kociolek et al. (2015) examined tendon gliding resistance (middle finger FDS tendon) to several workplace exposures concurrently: wrist posture, finger velocity, and loading. During finger flexion, a multiplicative posture-force effect was observed, with greater tendon frictional work during higher load conditions with a flexed wrist (93.0% increase) than neutral (33.5% increase). A main effect of velocity was also noted (58.0% increase from 50 to 150 mm/s). Increasing all three factors had an interactive effect on frictional work during finger extension, indicating simultaneous exposure to multiple workplace demands elevates risk of tendon-related MSDs beyond each individual factor. These findings parallel Goldstein, Armstrong, Chaffin, and Matthews (1987) who found amplified effects of the FDS and flexor digitorum profundus (FDP) tensile loads on shear force between the tendon sheath and adjacent tissues with deviated wrist postures (flexion > extension > neutral). Although frictional work is primarily conducted in cadavers, these biomechanical factors correspond with hypotheses and histological examinations on friction-induced injuries. Mechanical abrasion of the tendon and synovium can lead to fibrosis and fraying of the tendon, hypertrophy of the synovium, as well as potentially invoking an inflammatory response that may decrease tissue lubrication, leading to further degeneration and possible pathology (Armstrong et al., 1984; Kutsumi et al., 2005; Schuind et al., 1990; Smutz et al., 1994).

Tensile loads on the tendons are considered to be an integral biomechanical risk factor in the development of hand/wrist tendinitis (Armstrong et al., 1987; Moore et al., 1991). Tendons exhibit viscoelastic behavior, thus deforming proportional to tensile loads in a manner that is rate and duration dependent (Pradas & Calleja, 1990). To date, several studies have investigated the viscoelastic behavior of various tendons, with Goldstein et al. (1987) identifying the cyclic creep strain properties as a potentially significant factor in the etiology of hand/wrist tendinitis. Cyclically loading FDP tendons in a neutral wrist posture over 500 cycles under different loads, load durations, and periods, it was observed that tendons exhibited cumulative strain with an initial nonlinear deformation followed by a linear phase (Goldstein et al., 1987). Importantly, the experimental conditions represented a range of everyday force/repetition occupational exposures, with more strenuous loading parameters (i.e., increased load, longer load duration, and shorter recovery times) resulting in greater strain. Similarly, Smutz, France, and Bloswick (1995) observed greater, faster development of creep strain in the FDS and FDP tendons with higher loads. Static loading increased tendon strain, with the highest load condition (100 N) causing 2.2% to 2.3% total strain, predicted to result in chronic damage and potential tendinitis (Smutz et al., 1995). The results are consistent with several in vitro experiments reporting greater tendon damage, as evidenced by tissue microstructural and mechanical changes leading to eventual macroscopic failure (i.e., rupture) in response to cumulative strain from increasing tissue loads/stresses and higher cyclic frequency (Fung et al., 2009; Ker, Wang, & Pike, 2000; Schechtman & Bader, 1997; Wang & Ker, 1995; Wang, Ker, & Alexander, 1995; Wren, Lindsey, Beaupré, & Carter, 2003). Although these findings possess the usual limitations of in vitro testing, they corroborate biopsy findings in chronic tendinopathy samples (for a detailed review, see Shepherd & Screen, 2013) and tissue biochemical/morphological changes within in vivo animal-based models (see next paragraph). Measuring FDS and FDP tendon force using buckle transducers in vivo during carpal tunnel release surgery found that tendon forces are dependent on posture. Specifically, increasing finger flexion at the metacarpophalangeal (MP) joint resulted in greater tendon force during dynamic finger motion for the FDP, but only during flexed wrist postures for the FDS (Kursa, Lattanza, Diao, & Rempel, 2006). The greater tensile forces are believed to be needed to overcome passive extensor moments, co-contraction of agonist muscles, as well as tendon gliding resistance among other factors. As mentioned previously, gliding resistance is significantly increased with deviated wrist postures, suggesting that greater tensile load is required for the same external force, consequently increasing tendon strain. Contrary to their hypothesis, they found no difference in tendon force with fingertip loading rate (Kursa, Diao, Lattanza, & Rempel, 2005). Schuind, Garcia-Elias, Cooney, and An (1992) also measured in vivo tendon forces of the FDP, FDS, and flexor pollicis longus (FPL) during carpal tunnel surgery. High tendon forces were noted during pinching tasks (1.4–8.3 kg), corroborating the increased passive forces quantified during pinch grip (Keir, Wells, & Ranney, 1996). As a result, force, repetition, and posture are seen to play major roles in the development of tendinitis due to cumulative strain as a result of tensile stresses.

Although human-based studies provide biomechanical and physiological plausibility to the dose–response relationship, ethical concerns prohibit exposures from eliciting injury (Clark, Barr, Amin, & Barbe, 2004). In vivo animal studies have provided substantial evidence linking mechanics to the manifestation of tendon disorders by quantifying relationships between physical demands and tendon pathology in a controlled setting. A number of in vivo animal experiments have observed tendon degeneration, as evidenced by collagen disorganization, hypervascularity, microtears, and localized cellular indicators of cumulative damage, due to overuse activity (e.g., Backman, Boquist, Fridén, Lorentzon, & Toolanen, 1990; Barbe & Barr, 2006; Nakama, King, Abrahamsson, & Rempel, 2005, 2007; Soslowsky et al., 2000). Notably, Barbe et al. (2003), and Barr and Barbe (2002) developed an in vivo rat model of work-related MSD to voluntary forceful, repetitive upper extremity tasks. Rats were trained to perform a repetitive reaching/grasping task for 2 hr/day, 3 days/week to up to 12 weeks, with small cohorts euthanized every couple weeks to quantify progression. Auditory cues signaled rats of a new food pellet. Within 5 s of the cue, rats grasped and pulled a handle to receive their food pellet. Timing of auditory cues and force required were varied to simulate different workplace exposure levels of repetition rate and task force. Across a series of studies, they found a consistent relationship between more forceful and repetitive exertions on degeneration of the flexor digitorum tendons (i.e., fibrosis and thickening), localized forearm inflammatory responses, decreased grip strength, and sensorimotor decline (Abdelmagid et al., 2012; Barbe et al., 2003; Barbe et al., 2008; Elliott et al., 2009, 2008; Fedorczyk et al., 2010; Gao et al., 2013; Kietrys, Barr, & Barbe, 2011; Kietrys et al., 2012). Specifically assessing the interactive effects between force and repetition, Barbe et al. (2013) compiled 10 years of experimental data assessing biochemical, morphological, and sensorimotor responses to concurrent exposures to repetition (two or four reaches per minute) and force (15% or 60% maximum voluntary contraction [MVC]): low repetition-low force (LRLF), high repetition-low force (HRLF), low repetition-high force (LRHF), and high repetition-high force (HRHF) (analogous to Armstrong et al., 1987; Silverstein, Fine, & Armstrong, 1986, 1987). Several outcome measures displayed a multiplicative effect between repetition and force. Importantly, the HRHF group exhibited the most severe signs of flexor digitorum tendon pathology, greatest levels of stress and repair proteins localized to the forearm tendon, as well as extensive damage to the tendon fibrils. Similar fatigue-induced tendon degeneration results are observed during controlled in vivo animal models, where tendon loading is standardized using mechanical devices attached directly to animal limbs (e.g., Fung et al., 2010). Although these experiments were conducted in animals, it parallels the biomechanical plausibility from human-based experimental studies as well as epidemiological evidence, thus offering a strong argument for a dose–response relationship between workplace exposures and risk of hand/wrist tendon–related MSDs.

Summary—Tendon-Related Disorders

Based on epidemiological studies, there is consistent, positive evidence for a dose–response relationship between force exposure and risk of hand/wrist tendon–related MSDs in the workplace. Repetition and posture display inconsistent associations, although trends suggest a relationship. Combining workplace exposures exhibits a multiplicative effect on risk for injury. Low frequency of definitive tendon-related injuries and unequal representation of severe exposures is a significant limitation in deriving dose–response relationships epidemiologically. In contrast, human- and animal-based experimental studies provide strong dose–response evidence for each of the workplace risk factors with hand/wrist tendinitis and tenosynovitis. Higher levels of force, repetition, and deviated wrist/finger postures (particularly wrist flexion and pinching grips) increase tendon-tendon sheath frictional work and tensile stresses that can manifest in tendon pathology (animal studies) and is consistent with histological findings among humans. Overall, the biomechanical plausibility is consistent with the controlled lab-based animal experiments and the bulk of epidemiological studies indicative of a dose–response relationship between force, repetition, and posture on hand/wrist tendon–related MSDs.

Epicondylitis

Epicondylitis is highly prevalent in manually demanding occupations including forestry, food processing, and assembly lines due to exposure to forceful exertions, repetitive joint movements, awkward postures, vibrating tools, and/or combinations (Shiri & Viikari-Juntura, 2011). Individuals with epicondylitis experience pain radiating down the arm from the lateral or medial aspect of the elbow (Harrington, Carter, Birrell, & Gompertz, 1998; Piligian et al., 2000). Lateral epicondylitis (tennis elbow) is associated with irritation of the forearm extensor tendons at the lateral epicondyle of humerus, whereas medial epicondylitis (golfer’s elbow) is an injury at the origin of the pronator teres, palmaris longus, and/or flexor carpi radialis tendons at the medial epicondyle of humerus (Nirschl & Ashman, 2003). This section evaluates the dose–response relationship between the risk factors and epicondylitis, based on seven epidemiological and three experimental studies. Study OR, HR, and 95% CIs are compiled in Table 2.

Table 2

Summary of Workplace Epidemiological Evidence on Epicondylitis

Study	Design	Cohort	MSDs	Results
Haahr and Andersen (2003)	Case–control	483 (53% female)209 (52% female) had lateral epicondylitisAge: 18–66 years	Lateral epicondylitis based on physical examination	Force:Tools ≥1 kg vs. tools <1 kg OR: women = 2.8 [1.6, 5.0]; men = 2.2 [1.3, 3.9]Posture:Wrist deviation from neutral 25%–50% time vs. <25% time OR: women = 2.9 [1.6, 5.2] ≥75% time vs. <25% time OR: women = 10.0 [4.1, 22.4]; men = 3.2 [1.5, 6.9]Repetition:Repetitive finger or wrist movements ≥75% time vs. <25% time OR: women = 2.8 [1.4, 5.4]Vibration:Using vibrating tools 25%–50% time vs. <25% time OR: men = 2.8 [1.3, 5.9]
Shiri, Viikari-Juntura, Varonen, and Heliövaara (2006)	Cross-sectional	4,698 (53% female)63 (57% female) had lateral epicondylitis86 (71% female) had or possibly had medial epicondylitisAge: 30–64 years	Lateral and medial epicondylitis based on standardized health examination and self-reported symptoms	Medial epicondylitisForce:High handgrip ≥1 hr/day 1–8 years vs. none: OR = 2.2 [1.1, 4.3] ≥20 years vs. none: OR = 2.5 [1.4, 4.5]Repetition:Wrist flexion/extension for ≥2 hr/day 9–19 years vs. none: OR = 2.2 [1.1, 4.4] ≥20 years vs. none: OR = 3.6 [2.1, 6.2]Force and Repetition:Handling loads >5 kg for ≥2 times/min and ≥2 hr/day 1–8 years vs. none: OR = 2.4 [1.3, 4.5]Handling loads >20 kg, for ≥10 times/min 1–8 years vs. none: OR = 2.5 [1.4, 4.6] ≥20 years vs. none: OR = 2.3 [1.2, 4.2]Vibration:Using vibrating tools ≥2 vs. <2 hr/day: OR = 2.2 [1.1, 4.4]Lateral epicondylitisRepetition:Wrist flexion/extension for ≥2 hr/day
				9–19 years vs. none: OR = 2.4 [1.2, 4.9] ≥20 years vs. none: OR = 2.8 [1.4, 5.8]Force and Repetition:Handling loads >20 kg, for ≥10 times/min ≥20 years vs. none: OR = 2.6 [1.3, 5.1]
Fan et al. (2009)	Cross-sectional	733 (47.7% female)38 (63.2% female) had lateral epicondylitisAge: 18–65 yearsManufacturing and health care	Lateral epicondylitis based on physical examination	Force and Posture:Supination ≥45° (≥5% time) and forceful lifting vs. supination <5% time and no lifting OR = 3.43 [1.39, 8.51]Force and Repetition:Repetitive forceful tasks 1–5 times/min vs. <1 time/min: OR = 4.00 [1.44, 11.11] >5 times/min vs. <1 time/min: OR = 5.75 [2.03, 16.28]
Walker-Bone, Palmer, Reading, Coggon, and Cooper (2012)	Cross-sectional	6,038 (56% female)45 (54% female) had lateral epicondylitis34 (71% female) had medial epicondylitisAge: 25–64 years	Lateral and medial epicondylitis based on questionnaire and physical examination	Medial epicondylitisRepetition:Elbow extension/flexion >1 vs. <1 hr/day: OR = 5.1 [1.8, 14.3]Lateral epicondylitisRepetition:Elbow extension/flexion >1 vs. <1 hr/day: OR = 2.5 [1.2, 5.5]
Descatha, Dale, Jaegers, Herquelot, and Evanoff (2013)	Longitudinal	699 (36% female)34 (41.2% female) had lateral epicondylitis30 (40% female) had medial epicondylitisAge: 18+ yearsManufacturing, construction, biotechnology, and health care	Lateral and medial epicondylitis based on questionnaire and physical examination	Medial epicondylitisForce: Gripping ≥4 vs. <1 hr/day: OR = 3.8 [1.5, 9.6]Posture:Wrist deviation from neutral 2–4 vs. <1 hr/day: OR = 4.9 [1.1, 20.7] ≥4 vs. <1 hr/day: OR = 8.2 [2.4, 27.9]Repetition:Forearm rotation ≥4 vs. <1 hr/day: OR = 2.5 [1.0, 5.8]Lateral epicondylitisPosture:Wrist deviation from neutral ≥4 vs. <1 hr/day: OR = 4.4 [1.5, 13.1]Repetition:Forearm rotation
				≥4 vs. <1 hr/day: OR = 2.7 [1.2, 6.2]
Herquelot et al. (2013)	Cross-sectional	3,710 (42% female)90 (44% female) had lateral epicondylitis	Lateral epicondylitis based on physical examination	Force and Repetition:High physical exertion and repetitive elbow movements for ≥2 hr/day vs. light exertion and no elbow movement OR: men = 3.78 [1.85, 7.70]; women = 2.54 [1.12, 5.76]
Fan et al. (2014)	Longitudinal	611 (48% female)57 (63% female) had lateral epicondylitisAge: 18+ yearsOffice work, assembly work, wood product manufacturing	Lateral epicondylitis based on physical examination	Force and Posture:Forearm pronation ≥45° for ≥40% time + power grip vs. <40% time + no power grip HR = 2.8 [1.35, 5.77] ≥45° for ≥40% time + lifting loads ≥3% time vs. <40% time + no lifting HR = 2.5 [1.19, 5.24] ≥45° for ≥40% time + duty cycle ≥10% vs. <40% time of pronation + duty cycle <10 % HR = 2.25 [1.09, 4.66]

Note. MSDs = musculoskeletal disorders; OR = odds ratio; HR = hazard ratio.

Epidemiological Evidence

Force

An increased risk of epicondylitis with prolonged gripping or use of heavy tools was found in three studies. The OR for lateral epicondylitis was 2.2 (men) and 2.8 (women) using tools weighing 1 kg or more compared with using tools lighter than 1 kg (Haahr & Andersen, 2003). A 3-year longitudinal study found an OR = 3.8 for medial epicondylitis in workers performing handgrip tasks for at least 4 hr/day compared with durations shorter than 1 hr/day (Descatha, Dale, Jaegers, Herquelot, & Evanoff, 2013). In addition, the duration of employment in jobs involving forceful gripping was also found to influence the risk of epicondylitis. For instance, the ORs of medial epicondylitis were 2.2 and 2.5 in workers who applied high handgrip forces for at least 1 hr/day for 1 to 8 years and 20 or more years, respectively, compared with those without forceful gripping (Shiri, Viikari-Juntura, Varonen, & Heliövaara, 2006). Conversely, Walker-Bone, Palmer, Reading, Coggon, and Cooper (2012) suggested a lack of significant association between force and epicondylitis based on workers lifting loads more than 5 kg versus those who lifted lighter loads.

Repetition

Prolonged repetitive tasks involving the fingers, wrist, or elbow have been positively related to the risk of epicondylitis. The OR for lateral epicondylitis was 2.8 in female workers performing repetitive finger or wrist movements for at least 75% of the time versus less than 25% of time (Haahr & Andersen, 2003). Furthermore, epicondylitis in workers who performed repetitive wrist flexion-extension for at least 2 hr/day for 9 to 19 years had ORs of 2.2 (medial) and 2.4 (lateral), versus those not exposed to repetitive wrist flexion-extension (Shiri et al., 2006). The ORs for epicondylitis in workers with 20 or more years of repetitive wrist motion were 3.6 (medial) and 2.8 (lateral). Repetitive elbow flexion-extension for over 1 hr/day led to ORs of 5.1 (medial) and 2.5 (lateral) versus less than 1 hr/day (Walker-Bone et al., 2012). Similarly, ORs of 2.5 (medial) and 2.7 (lateral) were found in workers experiencing repetitive forearm rotation for at least 4 hr/day versus less than 1 hr/day (Descatha et al., 2013).

Posture

Two studies found a positive relationship between prolonged wrist deviation and epicondylitis. Awkward wrist postures sustained for 2 to 4 hr/day resulted in an OR of 4.9 for medial epicondylitis compared with less than 1 hr/day (Descatha et al., 2013). ORs of 8.2 (medial) and 4.4 (lateral) were found in workers with awkward wrist postures sustained for at least 4 hr/day. Furthermore, lateral epicondylitis incidence was greater in women who maintained awkward wrist postures for 25% to 50% compared with less than 25% of time (OR = 2.9) (Haahr & Andersen, 2003). The OR increased to 10 in women who had wrist deviation for 75% or more of their time. They also found an OR of 3.2 for lateral epicondylitis in men who sustained awkward wrist postures for at least 75% of time. The above studies suggest a dose–response relationship between non-neutral wrist posture and epicondylitis, although two studies did not observe such a relationship. Fan et al. (2009) found no increased risk of lateral epicondylitis from radial and ulnar deviation maintained for a minimum of 4% of time versus shorter than 4%. Similarly, there was no difference in risk of lateral epicondylitis in workers who exhibited flexed and extended wrists for at least 2% of time (at 45° or greater) and for at least 40% of time (at 15° or greater) than those postures for less than 2% and 40% of time, respectively (Fan et al., 2014).

Vibration

The relationship between long-term use of vibrating tools and epicondylitis is inconsistent. Shiri et al. (2006) found an OR of 2.2 (medial epicondylitis) in workers who used vibrating tools for at least 2 hr/day versus less than 2 hr/day. Using vibrating tools for 25% to 50% of time increased the OR of lateral epicondylitis in male workers by 2.8 times compared with less than 25% of time (Haahr & Andersen, 2003). Two studies suggest no significant relationship between vibration and epicondylitis (Herquelot et al., 2013; Walker-Bone et al., 2012). Lateral epicondylitis risk in workers using vibrating tools for greater than 2 hr/day did not differ from less than 2 hr/day (Herquelot et al., 2013). Similarly, no difference was found for medial or lateral epicondylitis in workers who used vibrating tools for greater than 1 hr/day compared with less than an hr/day (Walker-Bone et al., 2012).

Interaction between force and posture

Prolonged awkward forearm postures combined with forceful tasks have been associated with increased lateral epicondylitis risk. Fan et al. (2009) found forearm supination for at least 5% of time, combined with lifting loads of 4.5 kg or heavier, resulted in an OR of 3.4 (lateral epicondylitis) compared with forearm supination under 5% of time with no lifting. The same group found HRs of 2.3 to 2.8 with pronation for at least 40% of time combined with forceful exertions (Fan et al., 2014). Despite the significance of pronation and force, they did not find a combined effect with wrist deviation.

Interaction between Force and Repetition

Lateral epicondylitis was more likely in workers who performed forceful tasks for 1 to 5 times/min (OR = 4) and more than 5 times/min (OR = 5.75) compared with less than 1/min (Fan et al., 2009). Compared with lighter exertions, higher self-reported physical exertion combined with repetitive elbow flexion/extension for at least 2 hr/day had ORs of 2.5 (women) and 3.8 (men) for lateral epicondylitis (Herquelot et al., 2013). For medial epicondylitis, an OR of 2.4 was reported when loads more than 5 kg were handled at least 2 times/min and at least 2 hr/day for 1 to 8 years compared with those who did not perform those tasks (Shiri et al., 2006). Similarly, medial epicondylitis risk increased in workers who handled loads heavier than 20 kg, for at least 10 times/min for 1 to 8 years (OR = 2.5) and at least 20 years (OR = 2.3). They also found an OR of 2.6 for lateral epicondylitis in workers lifting loads heavier than 20 kg, for at least 10 times/min for 20 years or more.

Lab-Based Experimental Evidence

Repetition

There are few laboratory-based studies examining repetition and epicondylitis. Nakama et al. (2005, 2007) electrically stimulated the FDP muscles in rabbits and found more microtears in tendons stimulated for 60 repetitions/min than 10 repetitions/min over a total of 80 hr. There remains a need to investigate the effects of repetition rates on the primary muscles involved in medial epicondylitis such as pronator teres, palmaris longus, and flexor carpi radialis.

Force and posture

Lab-based investigations present insufficient evidence for a dose–response relationship between force combined with posture and epicondylitis. Regan, Wold, Coonrad, and Morrey (1992) examined the extensor carpi radialis brevis muscle (ECRB) tendon origin and found degenerative histopathological changes, such as vascular/fibroblastic proliferation and hyaline degeneration, in patients with lateral epicondylitis. This suggests that an injury to the ECRB tendon origin may lead to the development of lateral epicondylitis. Bunata, Brown, and Capelo (2007) observed that the undersurface of a cadaveric ECRB tendon origin rubbed against the lateral edge of the capitellum during elbow extension, suggesting greater risk of injury with repeated elbow movements. A cadaveric study by Tanaka et al. (2011) measured contact pressure between the ECRB tendon origin and the lateral edge of capitellum in a series of experimental conditions and found a significant increase in contact pressure with ECRB tendon force, elbow extension, forearm pronation, and varus torque. These findings suggest greater stress on the ECRB tendon leading to a higher risk of microtears and lateral epicondylitis. Contact pressure was greatest (107.2 ± 43.0 kPa) during full elbow extension, maximum forearm pronation, ECRB tendon force (19.6 N), with a varus torque, whereas the lowest pressure (0.2 ± 0.6 kPa) was recorded during 90° of elbow flexion, neutral forearm posture, with the absence of ECRB tendon force and varus torque. Although suggestive of a dose–response association, further in vivo studies are required to elucidate any relationship between force combined with deviated forearm/elbow posture and epicondylitis.

Summary—Epicondylitis

Based on epidemiological studies, the risk of epicondylitis is related to (a) repetitive elbow, wrist, or forearm movements and (b) high force combined with either high repetition or awkward forearm postures. However, epidemiological studies found inconsistent evidence for associations between epicondylitis and risk factors of (a) high force alone; (b) awkward wrist postures, with or without high force; and (c) vibration. Minimal lab-based experimental evidence was found and included only cadaveric and animal-based studies.

CTS

CTS is a common disorder of the hand and wrist caused by chronic compression of the median nerve. The carpal tunnel is bordered by eight carpal bones dorsally and the flexor retinaculum or transverse carpal ligament (TCL) on the palmar side. This space contains the median nerve and nine finger flexor tendons (FPL, four FDS, and four FDP). Increased carpal tunnel pressure (CTP) results in nerve compression and reduced nerve conduction. It is established that CTS patients typically have higher CTP than healthy individuals. Chronic compression leads to reduced nerve conductivity, resulting in the characteristic symptoms of CTS including pain, tingling, and numbness in the first three and a half fingers. CTS is commonly found in working populations with an estimated cost of medical care in the United States exceeding US$2 billion per year (Dale et al., 2013). Work-related risk factors such as force, repetition, posture, and vibration are often cited as influencing the development of CTS. The objective of this section is to assess the epidemiological and lab-based evidence of dose–response relationship between risk factors and the development of CTS.

Epidemiological Evidence

Force

Epidemiological studies generally agree there is a relationship between force and CTS risk (Table 3). Studies reviewed in the NIOSH review (Bernard, 1997) led to the conclusion that there was sufficient evidence of the work-relatedness of force on the development of CTS. In total, three studies since 1997 concur that force is a significant factor for CTS (Nathan, Istvan, & Meadows, 2005; Nordander et al., 2013; Thomsen, Hansson, Mikkelsen, & Lauritzen, 2002). Using right forearm extensor electromyography (EMG) to reflect force, Nordander et al. (2013) evaluated 2652 workers from a wide range of industries demonstrating that CTS prevalence was significantly higher in men exhibiting higher 10th and 90th percentile EMG, and with constrained movements compared with free work (Nordander et al., 2013). A study using video-based analysis to estimate force on a 5-point ordinal scale with verbal anchoring reported a higher risk in the working hand of various industrial workers with self-reported CTS symptoms (OR = 1.28) (Thomsen et al., 2002). However, this relationship was less clear for those with electrodiagnostically confirmed CTS (OR = 1.41, p = .174). Nathan et al. (2005) reported similar results in 148 industrial workers with medically confirmed CTS.

Table 3

Summary of Workplace Epidemiological Evidence on CTS

Study	Design	Cohort	MSDs	Results
Frost, Andersen, and Nielsen (1998)	Retrospective	743 (16.8% female) slaughterhouse and chemical factory workers398 controls (12.6% female)Age (all): 40.5 ± 12.2 years	CTS medically confirmedOccupational info obtained through questionnaire, observation, video recording	Vibration: exposure0 years: Observed cases: 1.6%1–5 years: O: 4.8%; PR = 3.04 [1.04, 8.910]; OR = 3.57 [1.13, 11.34]6–10 years: O: 7.6%; PR = 4.84 [1.92, 12.18]; OR = 5.34 [2.01, 14.20]11–15 years: O: 5.7%; PR = 3.60 [1.27, 10.20]; OR = 3.29 [1.10, 9.83]16–20 years: O: 7.1%; PR = 4.54 [1.32, 15.57]; OR = 4.18 [1.11, 15.80]>20 years: O: 6.3%; PR = 3.97 [1.44, 10.95]; OR = 4.44 [1.49, 13.22]
Thomsen, Hansson, Mikkelsen, and Lauritzen (2002)	Cross-sectional	731 workers	CTS through questionnaire, interview, or medically confirmed, for both working and nonworking hand	Repetition: (for working hand)Questionnaire case: OR = 1.21 [1.01, 1.46] (p = .039)Interview case: OR = 1.27 [1.01, 1.61] (p = .040)Medically confirmed case: OR = 1.84 [1.06, 3.19] (p = .030)Force: (for working hand)Questionnaire case: OR = 1.28 [1.08, 1.52] (p = .006)Interview case: OR = 1.12 [0.86, 1.48] (p = .400)Medically confirmed case: OR = 1.41 [0.86, 2.30] (p = .174)
Babski-Reeves and Crumpton-Young (2003)	Cross-sectional	53 fish-processing facility workers (94% female)	CTS through symptoms, positive provocative tests	Posture:Model 1 (mean wrist deviation): Radial/ulnar dev.: OR = 1.014 [0.975, 1.055] (p = .49) Flexion/extension: OR = 0.988 [0.955, 1.023] (p = .50) Pronation/supination: OR = 1.017 [0.986, 1.049] (p = .28)Model 2 (maximum wrist deviation): Radial dev.: OR = 0.991 [0.932, 1.054] (p = .78) Ulnar dev.: OR = 1.018 [0.960, 1.080] (p = .55) Flexion: OR = 1.00 [0.997, 1.002] (p = .87) Extension: OR = 0.953 [0.900, 1.010] (p = .10) Pronation: OR = 1.022 [0.991, 1.055] (p = .16) Supination: OR = 1.001 [1.00, 1.003] (p = .13)
Bovenzi, Della Vedova, Nataletti, Alessandrini, and Poian (2005)	Cross-sectional	100 controls,100 female furniture workers:Group 1 (n = 14) (orbital sanders): age: ~31 yearsGroup 2 (n = 76) (orbital + hand sanding): age: ~34 yearsGroup 3 (n = 10) (hand sanding): age: ~34 years	CTS through symptoms, positive provocative tests, 10 participants medically confirmedOccupational info through interviewsErgonomic evaluation using Strain Index	Vibration:Prevalence for controls: 8%Prevalence for furniture workers: 19%PR in furniture workers (controls as reference group):3.0 [1.3, 6.9] (p = .009)Group 1: PR (adjusted) = 3.8 [1.0, 13.7] (p = .04)Group 2: PR (adjusted) = 3.1 [1.3, 7.2] (p = .008)Group 3: PR (adjusted) = 1.5 [0.2, 12.0] (p = .65)
Violante et al. (2007)	Longitudinal (1-year results)	2092 (64.8% female)Age: ~38 years	CTS through questionnaire and medically confirmedOccupational exposure obtained through ergonomic assessment using ACGIH TLV	Repetition × Force<AL: OR = 1.0Between AL and TLV: OR = 1.5 [1.1, 2.0]>TLV: OR = 2.0 [1.5, 2.6]
Nathan, Istvan, and Meadows (2005)	Longitudinal baseline: 1984, follow-up: 2001/2002	148 industrial workers (40% female)Age (1984): ~35 yearsAge (2001/2): ~53 years	CTS medically confirmedOccupational info obtained through observation	Repetition: OR = 0.50 (p = .046)Force: OR = 3.50 (p = .064)
Nordander et al. (2013)	Cross-sectional	2652 (71% female)Age: ~40.9 years	Elbow, hand, wrist epicondylitis, CTSCTS through symptoms, positive provocative tests	Force: “static” (10th percentile), “peak” (90th percentile) (%/% MVE)Prevalence at 10th percentile Female: 0.35 (−1.2 to 1.7); male: 3.2 (1.3–6.3)Prevalence at 90th percentile Female: 0.19 (–0.04 to 0.4); male: 0.40 (0.04–0.7)Repetition: 10th, 50th, and 90th percentiles of angular distributionsWrist flexion (%/°): 10th percentile: NS 50th percentile: 0.28 (0.09–0.5) 90th percentile: 0.20 (0.01–0.4)Wrist angular velocity: % (°/s) 50th percentile: 0.20 (0.08–0.3)
Musolin, Ramsey, Wassell, and Hard (2014)	Cross-sectional	318 poultry processing workers (70% female)Age: ~39 years	CTS through symptoms and medically confirmedOccupational exposure obtained through ergonomic assessment using the ACGIH TLV	Repetition × ForcePrevalence of CTS by exposure group:Group 1 (<AL): 34%Group 2 (AL-TLV): 39% [0.76, 1.60] Adjusted PR = 1.16Group 3 (>TLV): 55% [1.20, 2.17] Adjusted PR = 1.61

Note. CTS = carpal tunnel syndrome; MSDs = musculoskeletal disorders; OR = odds ratio; ACGIH TLV = American Conference of Governmental Industrial Hygienists Threshold Limit Value; AL = action limit; PR = prevalence ratio; MVE = maximum voluntary excitation.

Repetition

Bernard (1997) concluded that there was epidemiological evidence of a positive association between repetitive work and CTS. Four epidemiological studies following the NIOSH report evidence of a dose–response between repetitive work and CTS (Latko et al., 1999; Nordander et al., 2013; Thomsen et al., 2002; Werner, Franzblau, Albers, & Armstrong, 1998) (Table 3). However, one study (Frost, Andersen, & Nielsen, 1998) reported a nonsignificant relationship, and another study reported a lower odd of developing CTS with repetitive hand movement (OR = 0.50), although both of these studies employed subjective methods (observation) to quantify hand repetitiveness. Using ACGIH HAL, a case-controlled study of 352 workers observed workplaces and videotapes of workers to rate the level of repetition on a 10-point VAS (Latko et al., 1999). A linear relationship was found between CTS symptoms and repetitiveness (low, medium, high), with symptoms increasing with each level of repetitive hand use (low 22%; high 46.5%). However, when electrodiagnostic criteria were used in conjunction with hand symptoms, the relationship was not significant (p = .06), with prevalences of 2.7% and 7.9% in the low and high repetition categories, respectively. A cross-sectional investigation of a number of manufacturing sectors using similar methods found gender and repetition as the most significant factors, accounting for 70% of the explained variance and resulting in an OR of 1.2 (Werner et al., 1998). Using electrogoniometers, Nordander et al. (2013) found CTS prevalence increased by 0.2% for every °/s increase in wrist angular velocity at the 50th percentile of wrist angular velocity in 423 workers. Similarly, higher risk was reported in the dominant or “working hand” of 731 workers when wrist electrogoniometers were used, with an OR of 1.21 in workers with self-reported CTS symptoms and an OR of 1.84 in medically confirmed CTS cases (Thomsen et al., 2002).

Posture

Epidemiological studies investigated in the NIOSH review concluded insufficient evidence for the association between extreme wrist posture and CTS. One epidemiological study conducted in 2003 also suggests there is insufficient evidence for the effect of wrist posture on CTS risk (Babski-Reeves & Crumpton-Young, 2003) (Table 3). In a cross-sectional study investigating 53 fish-processing facility workers, wrist postures were collected for 20 min using electrogoniometers and torsiometers while workers performed five normal work tasks. Two predictive models were developed: one based on mean wrist deviations and the other based on the maximum deviation in each direction. Results were largely inconclusive and dependent on the model used. For instance, although radial/ulnar deviation results in an OR = 1.014 when the model for mean wrist deviations was used, calculated odds were lower (OR = 0.991) for radial deviation and slightly higher (OR = 1.018) for ulnar deviation when the maximum deviation model was used.

Vibration

The NIOSH review provided evidence that exposure to vibrating tools increases the risk of CTS (Bernard, 1997). Since 1997, two epidemiological studies also provide evidence for the association between vibration exposure and CTS development (Bovenzi, Della Vedova, Nataletti, Alessandrini, & Poian, 2005; Frost et al., 1998) (Table 3). In a study of 100 female furniture plant workers, workers were split into three groups depending on the type of sanding typically performed: (A) orbital sanding only, (B) orbital sanding and hand-held sanding, or (C) only hand-held sanding. Vibrations were measured using accelerometers and daily vibration exposure was calculated as an 8-hr energy-equivalent frequency-weighted acceleration. The prevalence of CTS was significantly higher in the furniture workers (19%) compared with controls (8%), although not all CTS cases in the sample were clinically confirmed. The overall prevalence ratio (PR) for the furniture workers was 3.0 and was significantly greater in Group A (orbital sanders) (PR = 3.8) than in Group B (PR = 3.1) and Group C (PR = 1.5). An observational investigation in slaughterhouse workers found similar outcomes looking at the cumulative vibration exposure, with significantly greater odds and prevalence of CTS in exposed workers than in controls (Frost et al., 1998).

Interactive effects of risk factors

Significant evidence for the interaction between risk factors and risk of CTS has been reported (Bernard, 1997). Two studies using the ACGIH TLV for HAL report a significant association between repetition × force on developing CTS (Musolin, Ramsey, Wassell, & Hard, 2014; Violante et al., 2007). Violante et al. (2007) investigated various blue-collar workers at baseline and 12-month follow-up. At baseline, an ergonomic job assessment was carried out using the ACGIH TLV for HAL to classify workers into three groups of biomechanical load exposure. CTS cases were confirmed by questionnaires and nerve conduction studies. Workers in the “borderline” (between AL and TLV) and “unacceptable” (above TLV) groups had significantly greater odds of having CTS (borderline: OR = 1.5, unacceptable: OR = 2.0) compared with those in the “acceptable” (below AL) group. An investigation in 318 poultry processing plant workers also found greater prevalence of CTS in workers above the TLV (prevalence = 55%) compared with those between the AL and TLV (39%) or below AL (34%) (Musolin et al., 2014). After adjusting for sex, age, body mass index, and diabetes mellitus, the PR of workers in the above TLV group was significantly higher (PR = 1.61) compared with the AL-TLV group (PR = 1.16). However, only 42% of participants included in this analysis met their case definition of CTS which included a combination of questionnaire, symptom information, and nerve conduction study (NCS) results.

Lab-Based Experimental Evidence

Force

High hand and finger forces have been noted as significant contributors to the development of CTS. Animal studies (Clark et al., 2004; Smutz et al., 1994), cadaveric models (Keir, Wells, Ranney, & Lavery, 1997; Smutz et al., 1994), and several human studies (Ferguson, Fathallah, & Granata, 1993; Gabra, Gordon, Marquardt, & Li, 2016; Keir, Bach, & Rempel, 1998b; Marquardt, Gabra, & Li, 2015; Rempel, Keir, Smutz, & Hargens, 1997; Smith, Sonstegard, & Anderson, 1977; Werner, Elmqvist, & Ohlin, 1983) have examined the effects of force on the carpal tunnel. Human studies have demonstrated that CTP increases with finger force (Keir et al., 1998b; Rempel et al., 1997; Smith et al., 1977), and is further influenced by wrist posture (Rempel et al., 1997; Smith et al., 1977), and grip type (pinch or press) (Keir et al., 1998b). CTP has been shown to increase significantly and independently from wrist posture and described by a second-order polynomial (Rempel et al., 1997). A follow-up study indicated that CTP was approximately twofold greater when using a pinch versus finger pulp press up to 12 N (Keir et al., 1998b). Active tendon loading also increases volar movement of the FDS tendon, increasing contact between the tendon and the TCL seen using ultrasonography (Gabra et al., 2016). CTP increased three- to sixfold from baseline when muscles were stimulated depending on finger and wrist posture in 16 CTS patients during surgery (Werner et al., 1983). An ultrasound study of median nerve hypervascularization also demonstrated an influence of fingertip force on median nerve hemodynamics, as median nerve blood flow velocity was found to be significantly higher (3.6 cm/s) with 6 N of fingertip force compared with no force (2.8 cm/s) in 18 participants with and without CTS symptoms (Wilson, Tat, & Keir, 2017).

Cadaveric and animal studies allow greater experimental control to detail the effects of tendon force seen in human studies. Keir et al. (1997) found that cadaveric finger flexor tendons and palmaris longus loaded with 1 kg resulted in significantly higher pressures in the carpal tunnel than without load. In rats trained to perform a repetitive reach and grasping task for 2 hr/day, 3 days/week for 12 weeks at 50% to 70% of their maximum grip strength, visible accumulation of scar tissue and fat around the median nerve was noted, with increased levels of inflammatory macrophages compared with control rats (Clark et al., 2004). However, a study of two rhesus monkeys performing repetitive finger motion with one hand at a load of 20 N at 1 Hz for 6 hr/day, 5 days/week, for 3 weeks did not find changes in median nerve function (Smutz et al., 1994).

The effects of external force application have been noted in two cadaveric studies (Cobb, An, & Cooney, 1995; Kubo et al., 2018) and two human studies (Lundborg, Gelberman, Minteer-Convery, Lee, & Hargens, 1982; Szabo, Gelberman, Williamson, & Hargens, 1983). Using cadaveric arms, Cobb et al. (1995) found the highest CTP when external compression occurred directly over the carpal tunnel at the base of the palm. Similarly, Kubo et al. (2018) found a linear relationship between palmar contact force and CTP, regardless of FDS tension. Szabo et al. (1983) and Lundborg et al. (1982) used external palmar pressure to experimentally increase CTP, which resulted in reductions in median nerve function and the onset of CTS-like symptoms at 30 mmHg of internal fluid pressure (Lundborg et al., 1982), and complete sensory conduction block at 60 mmHg of internal fluid pressure (Lundborg et al., 1982; Szabo et al., 1983).

Repetition

Two studies with human subjects demonstrate the effects of repetitive hand mo-tion on CTP (Rempel, Manojlovic, Levinsohn, Bloom, & Gordon, 1994; Szabo & Chidgey, 1989). Rempel et al. (1994) found that CTP increased when moving cans 20 times/min (18 ± 3 mmHg) compared with baseline (8 ± 6 mmHg) and postactivity CTP (7 ± 6 mmHg), demonstrating the effects of highly repetitive motion. Szabo and Chidgey (1989) found that passive flexion-extension of the wrist (30 cycles/min for 1 min) significantly elevated CTP in the wrists of patients with early or intermediate CTS, but not for controls or advanced CTS patients. CTP was also significantly elevated for 10 min post-motion for early and intermediate CTS patients.

Finger movement velocity may play a role in the etiology of CTS through frictional forces during differential finger motion, leading to tissue fibrosis and reducing the space available for the median nerve, ultimately leading to compression of the nerve. High tendon velocities resulted in greater shear strain between finger flexor tendons and the SSCT due to greater differential motion between the SSCT and tendon (Tat, Kociolek, & Keir, 2015). Tendon-SSCT shear forces have been reported to increase in participants performing 30 min of differential repetitive finger flexion-extension movements (Tat et al., 2013). Oh et al. (2007) reported greater differential motion between the tendon and SSCT at velocities over 2.5 cm/s. In a cadaveric model of repeated cycles of finger movements, high velocities appeared to lower the damage threshold such that damage would occur at lower tendon excursions (Filius et al., 2014). Rat and primate studies demonstrate that animals trained to perform a repetitive task present immunohistochemical and morphological changes suggestive of damage. Al-Shatti, Barr, Safadi, Amin, and Barbe (2005) trained young rats to perform a highly repetitive reaching and grasping task over 3 to 8 weeks and found a significant increase in inflammatory cytokines in the wrist and forearm of the reaching limb, suggesting a role for cytokines in the pathophysiology of repetitive motion injuries. A study using four adult female monkeys trained to reach up to 8 hr/day using a 20% pinch grip and wrist flexion at 60° found a significant decrease in sensory nerve conduction velocity and increase median nerve cross-sectional area but not in cytokines (Smutz et al., 1994), contrary to evidence from rat studies (Sommerich et al., 2007).

Posture

Laboratory studies of CTP tend to support the effects of non-neutral wrist posture from epidemiological studies and further demonstrate the injury pathway. A comprehensive review of the effects of posture on CTP can be found in Vignais, Weresch, and Keir (2016). Using a wick catheter, Gelberman, Hergenroeder, Hargens, Lundborg, and Akeson (1981) found that CTP increased in both patients and controls in non-neutral wrist postures, more so in extension than flexion. Similar results have been reported using several other catheter techniques (Bauman, Gelberman, Mubarak, & Garfin, 1981; Rojviroj et al., 1990; Seradge, Jia, & Owens, 1995; Szabo & Chidgey, 1989; Werner et al., 1983) and in patients before and after endoscopic release surgery (Okutsu, Ninomiya, Hamanaka, Kuroshima, & Inanami, 1989). Unfortunately, many of these studies did not report wrist angles associated with “maximum” flexion and extension, making it difficult to determine a range of acceptable wrist posture. Werner, Armstrong, Bir, and Aylard (1997) measured wrist angles to find extreme wrist posture, particularly extension (60°–100°) and pronation, resulted in the largest CTP (26.8 ± 11.5 mmHg) compared with neutral (less than 20° flexion or extension) wrist and pronated forearm (8.3 ± 5.9 mmHg). Neutral wrist posture has been associated with the lowest compression of the median nerve based on median nerve diameter, flattening ratio and cross-sectional area using ultrasound (Kuo, Leong, Cheng, & Chang, 2001). Magnetic resonance imaging (MRI) has been used to demonstrate the finger flexor tendons migrated palmarly toward the TCL in flexion and dorsally in extension, changing tendon curvature between the postures, with the smallest radii in flexion with finger pinch force (Keir & Wells, 1999). Such results provide a mechanical basis of contact stress and friction on the median nerve from the surrounding tissues. Extreme wrist flexion (60°) has also been shown to result in the greatest shear strain between the flexor tendons and SSCT in cadavers (Yoshii et al., 2008). Wrist posture may also influence median nerve blood flow. Using high-frequency sonography, Wilson et al. (2017) found that blood flow velocity was significantly lower with a neutral wrist (2.9 cm/s) compared with 30° of flexion (3.4 cm/s), 15° flexion (3.3 cm/s), and 30° extension (3.3 cm/s). Nerve hemodynamics provide more detail for the interpretation of CTP by characterizing the type and direction of flow and specifying the location of nerve compression.

Finger posture has also been found to have a significant effect on CTP, independent from wrist posture. Rempel, Bach, Gordon, and So (1998) found that 0° (straight) wrist angle and 45° MP joint angle resulted in the lowest CTP. Similarly, Keir, Bach, and Rempel (1998a) found the lowest CTP was found with a neutral flexion/extension angle with relaxed fingers, with highest pressure with straight fingers and an extended wrist (Keir et al., 1998a). Pressures increased with increasing wrist extension angle, with straight fingers (0° MP) resulting in the highest overall pressures, approximately double those with MP at 45° (Keir et al., 1998a).

Summary—CTS

Epidemiological and experimental studies demonstrate positive graded associations between CTS and force, repetition and posture. Force and posture display strong, positive, dose-responses with CTP and effects on median nerve conduction. Both finger and wrist deviations are important. Laboratory studies have subsequently developed thresholds for injury risk based on wrist posture (Keir, Bach, Hudes, & Rempel, 2007) and a posture-based ergonomic tool (Weresch & Keir, 2018). Muscle, tendon, and externally applied forces affect CTP directly which in turn appear to alter nerve hemodynamics. Repetitive hand and finger movements result in histochemical and structural changes in finger flexor tendons, ultimately affecting tendon motion and median nerve conduction. Epidemiological studies suggest that risk factors are interactive and often multiplicative. Laboratory studies generally concur that the interaction effects between risk factors are significant in the development of CTS. The interaction between force and repetition is the most significant contributor to CTS, suggesting the importance of limiting highly repetitive and forceful work tasks.

Conclusion

In the workplace, the number of interceding factors and comorbidities make for complex dose-responses. Although not cause and effect, epidemiological studies provide the RRs of different factors on disorders which are often well evaluated in the laboratory, where detailed and controlled methods can elucidate the mechanisms by which these responses in the field occur. There is strong evidence for force playing a large role in the development and risk of hand/wrist tendon–related disorders, epicondylitis, and CTS. With respect to hand/wrist tendon–related disorders alone, there is insufficient epidemiological evidence for high repetition and deviated postures contributing to injury; however, mechanistic evidence from lab-based experiments observe a clear exposure-dependent response in biomechanical measures. Epidemiological and experimental studies agree that repetition, independent of other factors, is a significant contributor to epicondylitis. Epidemiological evidence also suggests that repetition and vibration play a significant dose–response dependent role in the risk of developing CTS, with inconclusive evidence for the role of wrist posture. However, laboratory studies provide experimental evidence for the contribution of force, repetition, and posture in the mechanisms of CTS development. Across all upper extremity MSDs, the presence of two or more exposures multiplies risk of injury. Future research should aim at standardizing the collection and reporting of exposure and outcome measures such that it is easier to facilitate the compilation and interpretation of different data sets. Doing so would allow us to better determine risk thresholds based on epidemiological and lab-based studies that will enable us to ultimately answer the question “how much is too much.” In light of the current evidence, it appears most important to limit exposure to forceful and repetitive tasks for workers to maintain worker health. The use of engineering controls, such as assistive devices, may permit the decrease in exposure risk, ensuring the longevity of worker well-being.

Key Points

Force is a significant risk factor for all upper extremity disorders; repetition is strongly associated with epicondylitis and CTS.

Exposure to multiple workplace risk factors results in multiplicative effects on upper extremity injury risk.

Combining controlled laboratory studies with epidemiology studies allows deeper delineation of the relationship and mechanisms from the often limited exposure variables in epidemiology studies.

Footnotes

ORCID iD

Peter J. Keir

Peter J. Keir received his PhD in kinesiology (biomechanics) from the University of Waterloo in 1995. He is a professor in the Department of Kinesiology at McMaster University in Hamilton, Ontario. His research examines upper extremity mechanics and function using EMG, imaging, and modeling to determine the mechanisms of work-related musculoskeletal disorders of the upper extremity.

Amanda Farias Zuniga received her MSc in kinesiology from McGill University (2015). She is a PhD candidate in the Department of Kinesiology at McMaster University. Her research focuses on upper extremity biomechanics, with an emphasis on imaging technologies.

Daanish M. Mulla received his MSc in kinesiology from McMaster University (2018). He is a PhD student in the Department of Kinesiology at McMaster University. His research focuses on upper extremity biomechanics.

Kumara G. Somasundram received a BS (kinesiology, honors) from McMaster University in 2017. He is an MSc student in the Department of Kinesiology (Occupational Biomechanics) at McMaster University. His research focuses on musculoskeletal modeling of the hand and wrist.

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