Vibration exposure and myocardial infarction incidence: the VHEEP case–control study (2024)

Article Navigation

Volume 56 Issue 5 August 2006

Article Contents

  • Abstract

  • Introduction

  • Aim

  • Methods

  • Results

  • Discussion

  • Conflicts of interest

  • References

  • < Previous
  • Next >

Journal Article

,

Bodil Björ

Correspondence to: Bodil Björ, Umea University, Umea SE-901 85, Sweden. e-mail: Bodil.bjor@envmed.umu.se

Search for other works by this author on:

Oxford Academic

,

Lage Burström

Search for other works by this author on:

Oxford Academic

,

Tohr Nilsson

Search for other works by this author on:

Oxford Academic

Christina Reuterwall

Search for other works by this author on:

Oxford Academic

Occupational Medicine, Volume 56, Issue 5, August 2006, Pages 338–344, https://doi.org/10.1093/occmed/kql024

Published:

22 May 2006

  • PDF
  • Split View
  • Views
    • Article contents
    • Figures & tables
    • Video
    • Audio
    • Supplementary Data
  • Cite

    Cite

    Bodil Björ, Lage Burström, Tohr Nilsson, Christina Reuterwall, Vibration exposure and myocardial infarction incidence: the VHEEP case–control study, Occupational Medicine, Volume 56, Issue 5, August 2006, Pages 338–344, https://doi.org/10.1093/occmed/kql024

    Close

Search

Close

Search

Advanced Search

Search Menu

Abstract

Objectives The main objectives of this study were to assess the risk of contracting first episode of myocardial infarction (MI) subsequent to vibration exposure and to assess a possible exposure–response relationship.

Methods The Västernorrland heart epidemiology programme (VHEEP, a part of the Stockholm heart epidemiology programme study) was the source of the data. VHEEP is a population-based case–control study of risk factors for acute MI. Exposure information was collected by questionnaire and vibration exposure was assessed in 218 cases and 257 controls. Relative risks were estimated using odds ratios (ORs) from binary logistic regression.

Results The results show that the OR of acute MI when exposed to vibration was 1.6 (95% CI: 1.1–2.4). It was not possible, however, to determine whether an exposure–response relationship was present.

Conclusions Working entailing vibrating machines is associated with an increased risk for acute MI.

Case–control, myocardial infarction, occupational, risk factor, vibration

Introduction

Risk factors for cardiovascular disease (CVD) have frequently been described and previously have predominantly been associated with lifestyle factors, hypertension, cholesterol level and gender [1]. Lately, studies have been published that deal with additional risk factors associated with the work environment [2–6]. Physical factors such as noise have been reported to be associated with an increased risk of CVD [7]. Noise exposure is often accompanied by exposure to vibration, which can influence the individual by being transmitted either through the hands (hand–arm vibration, HAV) or through the whole body (whole-body vibration, WBV) [8]. HAV exposure is associated with disorders in blood vessels, nerves, muscles and bones, while WBV exposure can lead to lower back pain [8–11]. Experimental studies have shown that exposure to vibration leads to elevated blood pressure (bp), changes in heart-rate variability and changes in peripheral vascular contraction [12–16]. Epidemiological studies of risk factors for acute myocardial infarction (MI) have shown a higher incidence of contracting hypertension among vibration-exposed individuals compared to unexposed controls [17,18]. Tamaian and Cocarla [19] have shown a higher prevalence of ischemic heart disease in vibration-exposed individuals than in unexposed controls. Studies specifically addressing the relationship between vibration exposure and MI have to our knowledge not yet been published in English-speaking journals.

Aim

The general aim of this study was to assess the risk of contracting acute MI in relation to various vibration-exposure characteristics. More specifically, the aims were to

  • (i) assess the risk of contracting MI in relation to vibration exposure and

  • (ii) assess the relation between level of exposure and response.

Methods

The Västernorrland heart epidemiology programme [VHEEP, a part of the Stockholm heart epidemiology programme (SHEEP) study] was the source of data. VHEEP is a population-based case–control study of risk factors for acute MI. The study base comprised all Swedish citizens living in the county of Västernorrland, who were 45–65 years of age and free from earlier clinically diagnosed MI. Cases were defined as all non-fatal and fatal first events of acute MI, first episode. Male and female cases and controls were identified during the period March 1993 to March 1995. The VHEEP study design is identical to that of the SHEEP study (previously described in detail [20–22]), differing only regarding regional catchment area and an additional set of questions covering exposure, among other things, to vibration.

Cases were identified from three sources and included at the time the disease occurred. The sources were (i) the coronary and intensive care units at the internal medicine departments of all the hospitals providing emergency treatment within the county of Västernorrland, (ii) the hospital discharge register for the same county and (iii) death certificates from the National Register of Causes of Death at Statistics Sweden. The criteria for determining MI were those accepted by the Swedish Association of Cardiologists in 1991.

One control per case was randomly selected from the study base after stratification for sex, age and hospital catchment area. The controls were selected within 2 days of case incidence from the computerized registers of the Västernorrland county population. Each control candidate was also checked for a history of MI since 1985 in the hospital discharge register for Västernorrland counties (as for cases). A waiting list of five control candidates per case were sampled simultaneously, so that a potentially non-responding control could be replaced by another, who was part of the study base at the time of case incidence. This substitution was made to maintain the power of the study and does not affect the non-participation rate. Before finally including a control in the study, case history information on previous MI was also requested. All controls were alive, regardless of whether or not the cases survived the MI. The routines and criteria for identification of cases and controls are described in detail elsewhere [5,20].

The exposure categorization was previously described in detail [20] and is thus only summarized here. Information on potential risk factors was collected by self-administered questionnaire. For deceased cases, exposure information was collected by a self-administered questionnaire completed by a close relative. This was administrated 6 months after the death of the individual case. In addition, hospital cases and their controls were offered a brief health examination including bp, blood samples and body measurements. This health examination was carried out no less than 3 months after inclusion in the study. Unless the subject explicitly declined to participate, up to four reminders were issued. All questionnaires were returned by mail. On receipt, they were checked and missing information was supplied during a telephone interview. Subjects, who stated in the questionnaire that they had suffered earlier MI, were contacted and interviewed regarding symptoms and treatment. If the information obtained suggested the occurrence of a previous clinically diagnosed MI, the subject was excluded from the study.

As described previously [20], data from both the questionnaire and the health examination were combined when the subjects were classified into exposure categories.

A vibration exposure assessment was conducted on an individual basis for both work and leisure time separately and together. The assessment was based on self-stated information on different occupations during lifetime and number of years spent in each occupation. This was combined with expert made estimations on daily exposure time and exposure magnitude in each occupation. The assessment for leisure time was based on self-reported type of vehicles/machines, number of exposed hours/day and number of exposed years.

The assessment of exposure magnitudes (frequency weighted acceleration) was based on type of vibration source reported (type of vehicle or vibrating tool) and expert estimations based on previously conducted measurements (in accordance with standard [9,10]).

Separate assessments were made for WBV and HAV and the estimated vibration value used for statistical analyses was the frequency weighted accumulated acceleration, calculated according to the formula:

\[a_{\mathrm{cum}}{=}{{\sum}_{i{=}1}^{n}}(a_{\mathrm{work}_{\mathrm{i}}})t_{i}\]

where acum = lifetime accumulated vibration acceleration (m h/s2); awork = acceleration during ith time period for worki (m/s2) and ti = duration of the acceleration awork for worki, i.e. hours/day × days/year × number of years at worki (h) [23,24]. The number of working days/year was set at 220 and n is the total number of jobs (up to 19 working periods in the study base). The accumulated frequency weighted acceleration for leisure time was calculated in a corresponding way.

The accumulated vibrations for work and leisure time were added together to give a total exposure for HAV and WBV, respectively.

To examine the possibility of an exposure–response relationship, each exposure group was divided into tertiles. For the group with combined HAV and WBV exposure, this division was made with indexation of tertiles for HAV and WBV tertiles, respectively. Subjects with low or medium exposure to both HAV and WBV were categorized as low exposed. Those with medium or high for either HAV or WBV were categorized as medium exposed, while those with high exposure for both HAV and WBV were categorized as high exposed.

The exposure categorization regarding the risk factors considered potential confounders in the present analyses [obesity: body mass index (BMI) ≥ 30; smoking: current, ex, no and high bp: 160/90] has been described previously [20].

The VHEEP study comprised only few women exposed to vibration. Thus, only men were included in the statistical analysis. Only cases and controls with complete information from the self-administered questionnaire were included in the analysis. Since diabetes is a highly contributory factor to vascular disease, people who stated in the questionnaire that they had diabetes and were treated with insulin (presumably diabetes Type I; nine cases and four controls) were not included in the statistical analysis. Still, we wanted to control for other possible forms of diabetes (e.g. diabetes Type II) and therefore included diabetes in the regression model. The diabetes variable included in the regression model defined diabetes Type II as those stating diabetes with drug treatment or diet control at the time of inclusion in the study.

Computer software SPSS® was used for the statistical analysis. Estimates of relative risks were based on odds ratios (ORs) from binary logistic regression. In what will be referred to as ‘Model 1’, only design variables were controlled for: age (in 5-year periods) and hospital catchment area. Furthermore, in ‘Model 2’, potential confounders as well as design variables were adjusted for, i.e. overweight, hypertension, smoking and diabetes. Stratified analyses were made for the two groups: (i) subjects exposed to HAV only and (ii) subjects exposed to both HAV and WBV. The number of subjects exposed to WBV only (e.g. sailors, engine drivers, stewardess) were four cases and 15 controls. This group was too small to form a single stratum in the analyses and did not suit the stratum with combined exposure to HAV and WBV. Therefore, this group was also excluded from analysis. To estimate the overall risk of contracting MI when vibration exposed, analysis was made for all those in groups (i) and (ii). Since the vibration exposure was skewed, the vibration dose is given as the median exposure rather than the mean.

Results

The participation rate was 85% among the cases and 82% among the referents. Further, information on lifetime occupational history (i.e. the basis for determining vibration exposure) was incomplete for 17 cases and 20 controls. Thus, the statistical analyses comprised 475 subjects, 218 cases (157 exposed, 61 non-exposed) and 257 controls (155 exposed, 102 non-exposed) (Table 1). Descriptive data on subjects as well as on potential confounders in the different exposure groups are given in Table 1. Table 2 shows the distribution of working time (years) in occupational groups for cases and controls, respectively. The most frequent vibration-exposed occupation was metal workers among both cases and controls. The non-vibration-exposed occupation most common among cases and controls was engineers. As shown in Table 3, the number of subjects exposed during occupation and/or leisure time is similar for cases and controls. The distribution between low, medium and high exposed are also similar for cases and controls. Table 4 shows descriptive information on accumulated lifetime vibration exposure for the two exposure groups only HAV and both HAV and WBV. Combining both exposure groups (only HAV and both HAV and WBV) yielded an overall estimated relative risk of 1.6 (95% CI: 1.1–2.4) of contracting MI if exposed to vibration during lifetime (not given in table).

Table 1.

Descriptive data on potential confounders for the non-exposed and the different exposure groups, respectively

Non-exposedHAVHAV and WBV
CasesControlsCasesControlsCasesControls
n6110259729883
Mean age (SD) (years)58.0 (6.2)58.0 (5.5)58.4 (5.1)58.4 (5.8)57.8 (5.9)57.8 (5.6)
Bp ≥ 160/90224026183332
BMI ≥ 3012151272014
Diabetes (Type II)335292
Non-smoker194218262524
Ex-smoker144013322532
Smoker282028144827
Non-exposedHAVHAV and WBV
CasesControlsCasesControlsCasesControls
n6110259729883
Mean age (SD) (years)58.0 (6.2)58.0 (5.5)58.4 (5.1)58.4 (5.8)57.8 (5.9)57.8 (5.6)
Bp ≥ 160/90224026183332
BMI ≥ 3012151272014
Diabetes (Type II)335292
Non-smoker194218262524
Ex-smoker144013322532
Smoker282028144827

Data are given as numbers of subjects.

Open in new tab

Table 1.

Descriptive data on potential confounders for the non-exposed and the different exposure groups, respectively

Non-exposedHAVHAV and WBV
CasesControlsCasesControlsCasesControls
n6110259729883
Mean age (SD) (years)58.0 (6.2)58.0 (5.5)58.4 (5.1)58.4 (5.8)57.8 (5.9)57.8 (5.6)
Bp ≥ 160/90224026183332
BMI ≥ 3012151272014
Diabetes (Type II)335292
Non-smoker194218262524
Ex-smoker144013322532
Smoker282028144827
Non-exposedHAVHAV and WBV
CasesControlsCasesControlsCasesControls
n6110259729883
Mean age (SD) (years)58.0 (6.2)58.0 (5.5)58.4 (5.1)58.4 (5.8)57.8 (5.9)57.8 (5.6)
Bp ≥ 160/90224026183332
BMI ≥ 3012151272014
Diabetes (Type II)335292
Non-smoker194218262524
Ex-smoker144013322532
Smoker282028144827

Data are given as numbers of subjects.

Open in new tab

Table 2.

Major occupational groups and working time (given as numbers of working years) among cases and controls, respectively

OccupationCasesControls
VibrationNo vibrationVibrationNo vibration
Metal workers781013210
Drivers70006970
Building construction workers49305850
Forestry workers57202720
Electricians39704230
Crane/truck drivers27304030
Farmers17902260
Caretakers9901440
Carpenters1100460
Mining workers630210
Dental personnel62040
Engineers070001216
Office personnel03460714
Teachers02520361
Paper mill workers02060354
Health care and social workers01610201
Chemical industry workers050096
Others1732114762448
OccupationCasesControls
VibrationNo vibrationVibrationNo vibration
Metal workers781013210
Drivers70006970
Building construction workers49305850
Forestry workers57202720
Electricians39704230
Crane/truck drivers27304030
Farmers17902260
Caretakers9901440
Carpenters1100460
Mining workers630210
Dental personnel62040
Engineers070001216
Office personnel03460714
Teachers02520361
Paper mill workers02060354
Health care and social workers01610201
Chemical industry workers050096
Others1732114762448

The table represents 100% of the total working time in the study population.

Open in new tab

Table 2.

Major occupational groups and working time (given as numbers of working years) among cases and controls, respectively

OccupationCasesControls
VibrationNo vibrationVibrationNo vibration
Metal workers781013210
Drivers70006970
Building construction workers49305850
Forestry workers57202720
Electricians39704230
Crane/truck drivers27304030
Farmers17902260
Caretakers9901440
Carpenters1100460
Mining workers630210
Dental personnel62040
Engineers070001216
Office personnel03460714
Teachers02520361
Paper mill workers02060354
Health care and social workers01610201
Chemical industry workers050096
Others1732114762448
OccupationCasesControls
VibrationNo vibrationVibrationNo vibration
Metal workers781013210
Drivers70006970
Building construction workers49305850
Forestry workers57202720
Electricians39704230
Crane/truck drivers27304030
Farmers17902260
Caretakers9901440
Carpenters1100460
Mining workers630210
Dental personnel62040
Engineers070001216
Office personnel03460714
Teachers02520361
Paper mill workers02060354
Health care and social workers01610201
Chemical industry workers050096
Others1732114762448

The table represents 100% of the total working time in the study population.

Open in new tab

Table 3.

Number of exposed subjects during occupation and/or leisure time, divided in the three categories low, medium and high exposed

Exposure groupCasesControls
OccupationLeisureOccupation and leisureOccupationLeisureOccupation and leisure
Low3911638101
Medium392114425
High3901043012
Total11713271251218
Exposure groupCasesControls
OccupationLeisureOccupation and leisureOccupationLeisureOccupation and leisure
Low3911638101
Medium392114425
High3901043012
Total11713271251218

Open in new tab

Table 3.

Number of exposed subjects during occupation and/or leisure time, divided in the three categories low, medium and high exposed

Exposure groupCasesControls
OccupationLeisureOccupation and leisureOccupationLeisureOccupation and leisure
Low3911638101
Medium392114425
High3901043012
Total11713271251218
Exposure groupCasesControls
OccupationLeisureOccupation and leisureOccupationLeisureOccupation and leisure
Low3911638101
Medium392114425
High3901043012
Total11713271251218

Open in new tab

Table 4.

Accumulated lifetime vibration exposure for the two different exposure groups

HAVHAV and WBV
CasesControlsCasesControls
HAVWBVHAVWBV
Number of exposed subjects59729883
Median (IQR)a9091 (2640–22 770)14 740 (6105–41 250)26 180 (13 850–51 535)5907 (1611–13 420)25 520 (15 400–54 160)4224 (1452–11 088)
HAVHAV and WBV
CasesControlsCasesControls
HAVWBVHAVWBV
Number of exposed subjects59729883
Median (IQR)a9091 (2640–22 770)14 740 (6105–41 250)26 180 (13 850–51 535)5907 (1611–13 420)25 520 (15 400–54 160)4224 (1452–11 088)

Data are given as median accumulated exposure (interquartile range, IQR) (m h/s2).

a

IQR = P25–P75.

Open in new tab

Table 4.

Accumulated lifetime vibration exposure for the two different exposure groups

HAVHAV and WBV
CasesControlsCasesControls
HAVWBVHAVWBV
Number of exposed subjects59729883
Median (IQR)a9091 (2640–22 770)14 740 (6105–41 250)26 180 (13 850–51 535)5907 (1611–13 420)25 520 (15 400–54 160)4224 (1452–11 088)
HAVHAV and WBV
CasesControlsCasesControls
HAVWBVHAVWBV
Number of exposed subjects59729883
Median (IQR)a9091 (2640–22 770)14 740 (6105–41 250)26 180 (13 850–51 535)5907 (1611–13 420)25 520 (15 400–54 160)4224 (1452–11 088)

Data are given as median accumulated exposure (interquartile range, IQR) (m h/s2).

a

IQR = P25–P75.

Open in new tab

Tables 5 and 6 show ORs for contracting MI in relation to the accumulated vibration dose during lifetime for the two exposure groups HAV only (Table 5) and combined exposure to HAV and WBV (Table 6). Based on accumulated lifetime dose, exposure to HAV increases the adjusted OR by ∼40% (Table 5) while exposure to both HAV and WBV increases the risk of MI by >80% (Table 6).

Table 5.

ORs for accumulated lifetime exposure (m h/s2), divided into tertiles, for the group exposed to only HAV

ORmodel195% CInORmodel295% CIn
CasesControlsCasesControls
Only HAV exposed
    Non-exposed161102159102
    Low1.920.98–3.7923201.670.79–3.532120
    Medium1.450.74–2.8620231.630.78–3.401923
    High0.920.46–1.8416290.990.48–2.051629
Overall risk, regardless of exposure level1.370.86–2.1959721.380.83–2.285672
ORmodel195% CInORmodel295% CIn
CasesControlsCasesControls
Only HAV exposed
    Non-exposed161102159102
    Low1.920.98–3.7923201.670.79–3.532120
    Medium1.450.74–2.8620231.630.78–3.401923
    High0.920.46–1.8416290.990.48–2.051629
Overall risk, regardless of exposure level1.370.86–2.1959721.380.83–2.285672

ORmodel1: controlled for hospital catchment area and age (5-year intervals). ORmodel2: adjusted for overweight, hypertension, smoking, diabetes (Type II), hospital catchment area and age.

Open in new tab

Table 5.

ORs for accumulated lifetime exposure (m h/s2), divided into tertiles, for the group exposed to only HAV

ORmodel195% CInORmodel295% CIn
CasesControlsCasesControls
Only HAV exposed
    Non-exposed161102159102
    Low1.920.98–3.7923201.670.79–3.532120
    Medium1.450.74–2.8620231.630.78–3.401923
    High0.920.46–1.8416290.990.48–2.051629
Overall risk, regardless of exposure level1.370.86–2.1959721.380.83–2.285672
ORmodel195% CInORmodel295% CIn
CasesControlsCasesControls
Only HAV exposed
    Non-exposed161102159102
    Low1.920.98–3.7923201.670.79–3.532120
    Medium1.450.74–2.8620231.630.78–3.401923
    High0.920.46–1.8416290.990.48–2.051629
Overall risk, regardless of exposure level1.370.86–2.1959721.380.83–2.285672

ORmodel1: controlled for hospital catchment area and age (5-year intervals). ORmodel2: adjusted for overweight, hypertension, smoking, diabetes (Type II), hospital catchment area and age.

Open in new tab

Table 6.

ORs for accumulated lifetime exposure (m h/s2), divided into tertiles, for the group exposed to both HAV and WBV

ORmodel195% CInORmodel295% CIn
CasesControlsCasesControls
HAV and WBV exposed
    Non-exposed161102159102
    Low1.881.06–3.3037331.821.00–3.323633
    Medium1.991.16–3.4144372.001.13–3.554336
    High2.190.99–4.8117131.470.63–3.461513
Overall risk, regardless of exposure level1.971.28–3.0498831.841.16–2.909482
ORmodel195% CInORmodel295% CIn
CasesControlsCasesControls
HAV and WBV exposed
    Non-exposed161102159102
    Low1.881.06–3.3037331.821.00–3.323633
    Medium1.991.16–3.4144372.001.13–3.554336
    High2.190.99–4.8117131.470.63–3.461513
Overall risk, regardless of exposure level1.971.28–3.0498831.841.16–2.909482

ORmodel1: controlled for hospital catchment area and age (5-year intervals). ORmodel2: adjusted for overweight, hypertension, smoking, diabetes (Type II), hospital catchment area and age.

Open in new tab

Table 6.

ORs for accumulated lifetime exposure (m h/s2), divided into tertiles, for the group exposed to both HAV and WBV

ORmodel195% CInORmodel295% CIn
CasesControlsCasesControls
HAV and WBV exposed
    Non-exposed161102159102
    Low1.881.06–3.3037331.821.00–3.323633
    Medium1.991.16–3.4144372.001.13–3.554336
    High2.190.99–4.8117131.470.63–3.461513
Overall risk, regardless of exposure level1.971.28–3.0498831.841.16–2.909482
ORmodel195% CInORmodel295% CIn
CasesControlsCasesControls
HAV and WBV exposed
    Non-exposed161102159102
    Low1.881.06–3.3037331.821.00–3.323633
    Medium1.991.16–3.4144372.001.13–3.554336
    High2.190.99–4.8117131.470.63–3.461513
Overall risk, regardless of exposure level1.971.28–3.0498831.841.16–2.909482

ORmodel1: controlled for hospital catchment area and age (5-year intervals). ORmodel2: adjusted for overweight, hypertension, smoking, diabetes (Type II), hospital catchment area and age.

Open in new tab

The main effect of adjustment for potential confounders was a reduced risk estimate in the subgroup ‘high exposed’ among those exposed to both HAV and WBV (Tables 5 and 6, comparing Model 1 and Model 2 analyses).

Discussion

The results show that work-entailing exposure to vibration is associated with an increased risk of acute MI. The risk increment is statistically significant for the group exposed to both HAV and WBV (1.84; CI: 1.16–2.90), but not for the group exposed to HAV only (1.38; CI: 0.83–2.28). Analyses were also made on exposure closer in time to infarction (12 months preceding inclusion). The overall risks were similar for accumulated lifetime exposure and exposure closer in time to infarction. This might be due to that the subjects exposed at the time of inclusion also had been exposed before, making it difficult to determine if more resent or past exposure contributes most to the risk.

When examining the tertile analysis for the combined exposure group, no exposure–response relation is found (Table 6) and for the group exposed to HAV only, the tertile analysis suggests an inverse exposure–response relationship (Table 5). Considering overall risk, regardless of exposure level, the group exposed to both HAV and WBV has a higher accumulated vibration exposure than those exposed to HAV only (Table 4). The combined exposure group had a slightly higher OR (1.84, Table 6) than the group exposed to HAV only (1.38, Table 5), which itself may indicate an exposure–response relation.

The vibration-exposed occupation groups most frequently represented in this study were metal workers, professional drivers, building construction and forestry workers. Several occupations within these groups are exposed to high workload, often in combination of little ability to control the work situation, and are mainly blue-collar workers from lower social class. High workload as well as having a blue-collar occupation has been studied and found to be risk factors for MI [25]. However, the individual risk factors (e.g. obesity, smoking) that are more common among lower social classes are adjusted for in regression model 2. Although we had information on both workload and socio-economic status, it could not be used in the present regression analyses. One reason was that workload exposure information was restricted to the last 5 years of occupational activity before inclusion, while the vibration exposure was accumulated from start of occupational career.

The reason for not including socio-economic status was that cases as well as controls could have changed between blue- and white-collar work during their occupational careers.

As seen in Table 3, 25% of the cases and 19% of the controls have either only leisure time exposure or combined leisure time and occupational exposure. Due to the rather low frequency and the similarity in frequency between cases and controls, the leisure time exposure is not likely to contribute to the risk increment for the cases compared to the controls.

We found an OR of 1.8 among the combined exposure group compared to an OR of 1.4 among the group exposed to only HAV. This higher risk could be explained either by the higher accumulated exposure level or by possible risks associated with certain areas of employment included. Previous studies show an increased risk of MI among bus drivers [26], who, among several other risk factors, are also exposed to WBV. Since our combined exposure group included bus and/or truck drivers, this might explain the higher risk in this group compared to the group exposed to a single form of vibration. Although, when subjects working as drivers at the time of inclusion were excluded in the regression model in a subanalysis, the OR increased from 1.45 to 1.76 (95% CI: 1.13–2.74). Thus in this study, it does not seem that drivers are at higher risk of contracting MI than those engaged in other vibration-exposed occupations.

Occupations associated with vibration exposure often imply exposure also to other environmental hazards, such as noise and exhaust fumes and particles from engines. Noise has repeatedly been reported as a comprising risk for MI [7]. There is a high level of association between exposure to noise and exposure to vibration, thus these exposures are difficult to separate in exposure assessment. The two exposures were not separated in this study; thus, the results might be interpreted as an effect due to noise and/or vibration exposure. There are studies showing that vibration exposure affects the autonomous nervous system [27,28] and can thereby give rise to changes in bp and vascular contraction. The association between vibration and noise exposure and disturbances to the autonomous nervous system is supported by Palmer et al. [29], who show an increased risk of severe hearing loss among those suffering from Raynaud's phenomena.

Engine exhaust is associated with MI [30] and the risk might be mediated by the effect of particles [31]. Several of the jobs in this study involve exposure to noise, exhaust and/or particles, but this has not been controlled for in the regression model.

About 10% of the cases were deceased, thus information on exposure for these individuals was collected from a close relative. This proxy information may be somewhat less precise than data collected from the exposed persons themselves. However, overstatement of vibration exposure among the cases is less likely since exposure to vibration is not a well-known risk factor of MI. Thus, this potentially less accurate exposure assessed group of individuals is not likely to contribute to an overestimation of the risk of MI. Pain in the upper extremities is a common symptom of MI. Since upper extremity pain also may occur in connection with drilling and other heavy work tasks associated with vibration exposure, vibration-induced incidences of MI may, in theory, remain undetected. However, with the case inclusion criteria applied, and when including also deceased cases, we do not think that such a selection bias exists in the present study.

The participation rate must be considered satisfactory and is almost equal for cases and controls. Information on occupational history was missing for a low proportion of the participating subjects, equal for cases and controls. Further, we have no reason to believe that non-participation was related to vibration exposure in a systematic way. Altogether, we do not think that the information loss affects the risk estimates to any larger extent.

The used method for estimating the vibration exposure may be influenced by recall bias both for number of years in each occupation, exposure time and type of vehicle/vibrating tool used. Furthermore, there are variations in vibration magnitude within an occupation, which may have affected the total accumulated lifetime vibration exposure. Although not based on specific measurements, epidemiological studies have shown that the reliability in this type of data is acceptable [32].

Conflicts of interest

None declared.

The Swedish Council for Working Life and Social Research, Sweden, provided financial support for this study.

References

1.

Braunwald E. Heart Disease, 4th edn, vol. 2. Philadelphia, PA: W. B. Saunders Company,

1992

; 887–1874.

2.

Kristensen TS. Work environment and cardiovascular diseases. A short review of the literature.

J Uoeh

1989

;

11

(Suppl.):

120

–133.

3.

Kristensen TS. Cardiovascular diseases and the work environment. A critical review of the epidemiologic literature on nonchemical factors.

Scand J Work Environ Health

1989

;

15

:

165

–179.

4.

Kristensen TS. Cardiovascular diseases and the work environment. A critical review of the epidemiologic literature on chemical factors.

Scand J Work Environ Health

1989

;

15

:

245

–264.

5.

Knutsson A, Hallquist J, Reuterwall C, Theorell T, Akerstedt T. Shiftwork and myocardial infarction: a case-control study.

Occup Environ Med

1999

;

56

:

46

–50.

6.

Olsen O, Kristensen TS. Impact of work environment on cardiovascular diseases in Denmark.

J Epidemiol Community Health

1991

;

45

:

4

–9; Discussion 9–10.

7.

Ising H, Babisch W, Kruppa B, Lindthammer A, Wiens D. Subjective work noise: a major risk factor in myocardial infarction.

Soz Praventivmed

1997

;

42

:

216

–222.

8.

Mansfield NJ. Human response to vibration. Bocaraton, FL: CRC Press LLC,

2005

; 227.

9.

ISO. ISO 2631, Mechanical Vibration and Shock—Evaluation of Human Exposure to Whole-Body Vibration. Geneva, Switzerland: International Organization for Standardization,

1997

.

10.

ISO. ISO 5349-1, Mechanical Vibration—Measurement and Evaluation of Human Exposure to Hand-Transmitted Vibration—Part 1: General Guidelines. Geneva, Switzerland: International Organization for Standardization,

2001

.

11.

Bovenzi M, Hulshof CT. An updated review of epidemiologic studies on the relationship between exposure to whole-body vibration and low back pain (1986–1997).

Int Arch Occup Environ Health

1999

;

72

:

351

–365.

12.

Nakamura H, Nakamura H, Nohara S, Okada A. Assessment of peripheral circulatory function in workers exposed to hand–arm vibration using non-invasive monitoring system for skin blood flow. In: Okada A, Taylor W, Dupuis H, ed. Hand–Arm Vibration. Kanazawa, Japan: Kyoei Press,

1990

; 195–199.

13.

Bovenzi M. Vibration white finger, digital blood pressure, and some biochemical findings on workers operating vibrating tools in the engine manufacturing industry.

Am J Ind Med

1988

;

14

:

575

–584.

14.

Bovenzi M. Digital arterial responsiveness to cold in healthy men, vibration white finger and primary Raynaud's phenomenon.

Scand J Work Environ Health

1993

;

19

:

271

–276.

15.

Bovenzi M. Finger systolic blood pressures during cold provocation in vibration exposed workers employed in selected industrial activities. In: Griffin M, ed. UK Group Meeting on Human Response to Vibration. Southampton, England: Human Factors Research Unit, Institute of Sound and Vibration, University of Southampton,

1997

.

16.

Bovenzi M. Vibration-induced white finger and cold response of digital arterial vessels in occupational groups with various patterns of exposure to hand-transmitted vibration.

Scand J Work Environ Health

1998

;

24

:

138

–144.

17.

Idzior-Walus B. Coronary risk factors in men occupationally exposed to vibration and noise.

Eur Heart J

1987

;

8

:

1040

–1046.

18.

Gobbato F, Blasina G, Crupi A, Patussi V. May hand-arm vibration exposure be a hypertension-risk factor? [author's translation].

Med Lav

1981

;

72

:

389

–398.

19.

Tamaian L-D, Cocarla A. Occupational exposure to vibration and ischemic heart disease.

J Occup Health

1998

;

40

:

73

–76.

20.

Reuterwall C, Hallqvist J, Ahlbom A et al. Higher relative, but lower absolute risks of myocardial infarction in women than in men: analysis of some major risk factors in the SHEEP study. The SHEEP Study Group.

J Intern Med

1999

;

246

:

161

–174.

21.

Ahlbom A, Feychting M, Gustavsson A et al. Occupational magnetic field exposure and myocardial infarction incidence.

Epidemiology

2004

;

15

:

403

–408.

22.

Hallqvist J, Lundberg M, Diderichsen F, Ahlbom A. Socioeconomic differences in risk of myocardial infarction 1971–1994 in Sweden: time trends, relative risks and population attributable risks.

Int J Epidemiol

1998

;

27

:

410

–415.

23.

Burström L, Lundström R, Hagberg M, Nilsson T. Comparison of different measures for hand–arm vibration exposure.

Safety Science

1998

;

28

:

3

–14.

24.

Griffin MJ, Bovenzi M, Nelson CM. Dose–response patterns for vibration-induced white finger.

Occup Environ Med

2003

;

60

:

16

–26.

25.

Belkic KL, Landsbergis PA, Schnall PL, Baker D. Is job strain a major source of cardiovascular disease risk?

Scand J Work Environ Health

2004

;

30

:

85

–128.

26.

Alfredsson L, Hammar N, Hogstedt C. Incidence of myocardial infarction and mortality from specific causes among bus drivers in Sweden.

Int J Epidemiol

1993

;

22

:

57

–61.

27.

Nakamoto M. Responses of sympathetic nervous system to cold exposure in vibration syndrome subjects and age-matched healthy controls.

Int Arch Occup Environ Health

1990

;

62

:

177

–181.

28.

Virokannas H. Cardiovascular reflexes in workers exposed to hand-arm vibration.

Kurume Med J

1990

;

37

(Suppl.):

S101

–S107.

29.

Palmer KT, Griffin MJ, Syddall HE, Pannett B, Cooper C, Coggon D. Raynaud's phenomenon, vibration induced white finger, and difficulties in hearing.

Occup Environ Med

2002

;

59

:

640

–642.

30.

Gustavsson P, Plato N, Hallqvist J et al. A population-based case-referent study of myocardial infarction and occupational exposure to motor exhaust, other combustion products, organic solvents, lead, and dynamite. Stockholm Heart Epidemiology Program (SHEEP) Study Group.

Epidemiology

2001

;

12

:

222

–228.

31.

Sjogren B. Occupational exposure to dust: inflammation and ischaemic heart disease.

Occup Environ Med

1997

;

54

:

466

–469.

32.

Bovenzi M. Exposure-response relationship in the hand–arm vibration syndrome: an overview of current epidemiology research.

Int Arch Occup Environ Health

1998

;

71

:

509

–519.

© The Author 2006. Published by Oxford University Press on behalf of the Society of Occupational Medicine. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Issue Section:

Original Papers

Download all slides

Advertisem*nt

Citations

Views

17,907

Altmetric

More metrics information

Metrics

Total Views 17,907

17,549 Pageviews

358 PDF Downloads

Since 11/1/2016

Month: Total Views:
November 2016 1
February 2017 2
March 2017 4
August 2017 3
October 2017 7
November 2017 5
December 2017 19
January 2018 13
February 2018 16
March 2018 14
April 2018 9
May 2018 31
June 2018 28
July 2018 21
August 2018 29
September 2018 20
October 2018 12
November 2018 20
December 2018 13
January 2019 20
February 2019 31
March 2019 27
April 2019 43
May 2019 38
June 2019 24
July 2019 22
August 2019 44
September 2019 48
October 2019 55
November 2019 98
December 2019 121
January 2020 141
February 2020 136
March 2020 162
April 2020 144
May 2020 106
June 2020 155
July 2020 172
August 2020 264
September 2020 324
October 2020 366
November 2020 330
December 2020 464
January 2021 394
February 2021 565
March 2021 479
April 2021 421
May 2021 492
June 2021 340
July 2021 397
August 2021 419
September 2021 460
October 2021 453
November 2021 323
December 2021 260
January 2022 310
February 2022 449
March 2022 498
April 2022 596
May 2022 458
June 2022 357
July 2022 437
August 2022 453
September 2022 451
October 2022 504
November 2022 465
December 2022 418
January 2023 425
February 2023 312
March 2023 309
April 2023 216
May 2023 166
June 2023 177
July 2023 266
August 2023 216
September 2023 155
October 2023 186
November 2023 206
December 2023 194
January 2024 364
February 2024 359
March 2024 355

Citations

Powered by Dimensions

11 Web of Science

Altmetrics

×

Email alerts

Article activity alert

Advance article alerts

New issue alert

Subject alert

Receive exclusive offers and updates from Oxford Academic

Citing articles via

Google Scholar

  • Latest

  • Most Read

  • Most Cited

Professor John Malcolm Harrington - obituary
A review of the injuries caused by occupational footwear
False-positive HIV screening test in a healthcare student
New occupational medicine competency framework for UK undergraduate medical students
Job demands and DHEA-S levels: a study on healthcare workers

More from Oxford Academic

Medicine and Health

Occupational Medicine

Books

Journals

Advertisem*nt

Vibration exposure and myocardial infarction incidence: the VHEEP case–control study (2024)

FAQs

Can vibration cause heart problems? ›

Experimental studies have shown that exposure to vibration leads to elevated blood pressure (bp), changes in heart-rate variability and changes in peripheral vascular contraction [12–16].

What are the side effects of whole-body vibration? ›

Whole-body vibration can cause fatigue, stomach problems, headache, loss of balance and "shakiness" shortly after or during exposure. The symptoms are similar to those that many people experience after a long car or boat trip.

Can vibrations cause nerve damage? ›

Hand–arm vibration syndrome (HAVS) is an occupational disorder caused by years of exposure to hand-transmitted vibration from powered tools. Patients with late-stage HAVS have peripheral neuropathy with loss of nerve fibers.

Can vibration remove plaque from arteries? ›

The 12-week vibration training significantly reduced aortic plaque areas, serum LDL, VLDL, ox-LDL, and IGF-1 levels in the AS mice model. Moreover, IL-6, phosphorylation of IGF-1R, and ERK significantly declined in the aorta as well in the WBV group. However, acute induced WBV increased IGF-1 in the blood.

What vibration frequency is harmful to humans? ›

Conclusion. Low-frequency (<20 Hz) or very high-frequency (>70 Hz) vibrations can be considered most dangerous for the human body. These vibrations can be found in vehicles (<20 Hz), in air transportation (0.2–7 Hz), or in heavy machine equipment (>20 Hz).

Who should not use whole body vibration? ›

People should avoid using whole body vibrating machines include those with the following: Heart diseases. History of heart attack or stroke. Pacemaker for heart conditions.

Is Body Vibration good or bad for you? ›

It's not yet clear if whole-body vibration provides the same range of health benefits as exercise you actively engage in, such as walking, biking or swimming. Some research does show that whole-body vibration may help improve muscle strength and that it may help with weight loss when you also cut back on calories.

Is whole body vibration good for your heart? ›

WBV training appears to be a useful therapeutic intervention to improve cardiac autonomic function in different populations, mainly through decreases in sympathovagal balance.

What is vibration syndrome? ›

Vibration syndrome has adverse circulatory and neural effects in the fingers. The signs and symptoms include numbness, pain, and blanching (turning pale and ashen). Of particular concern is evidence of advanced stages of vibration syndrome after exposures as short as one year.

What are three disadvantages of vibration? ›

Exposure to vibration could have a negative effect on the health of your employees. It could damage joints, muscles, circulation and sensory nerves. This could lead to considerable pain, time off or even disability.

What is white finger syndrome? ›

Vibration white finger is an occupational condition that results from long-term power tool use. Repeated vibration can damage blood vessels and result in symptoms such as white-coloring or paleness of the fingertips, numbness of the fingers and hands, weakness of the hands, and a loss of fine motor skills.

Is vibration good for heart? ›

Thus, vibration training could reduce the risk of sudden death during ischemia, through both attenuation of the ischemia-induced arrhythmia and facilitation of spontaneous defibrillation.

Can vibrations cause heart palpitations? ›

The heart rate was observed to be greatly increased when the subject was exposed to a vibration level of 5 m/s 2 . An increased heart rate of more than 90 beats per minute resulted in the subject's becoming aware of his heart rate and complaining of it as palpitation.

Who should not use vibration therapy? ›

Any current or recent blood clots (acute thrombosis conditions) • If you have a pacemaker • If you are pregnant • If you suffer with dizziness or inner ear problems Also if you have advanced osteoporosis with several spinal fractures, have had joint replacements such as hip or knee or if you have significant ...

Is mobile vibration harmful for heart? ›

No, not harmful. Patient's with pacemaker should avoid carrying cell phone in pockets near the pacemaker. Suggestions offered by doctors on Lybrate are of advisory nature i.e., for educational and informational purposes only.

Top Articles
Latest Posts
Article information

Author: Kieth Sipes

Last Updated:

Views: 6233

Rating: 4.7 / 5 (67 voted)

Reviews: 82% of readers found this page helpful

Author information

Name: Kieth Sipes

Birthday: 2001-04-14

Address: Suite 492 62479 Champlin Loop, South Catrice, MS 57271

Phone: +9663362133320

Job: District Sales Analyst

Hobby: Digital arts, Dance, Ghost hunting, Worldbuilding, Kayaking, Table tennis, 3D printing

Introduction: My name is Kieth Sipes, I am a zany, rich, courageous, powerful, faithful, jolly, excited person who loves writing and wants to share my knowledge and understanding with you.