I welcome the caution shown by Amick (1) in his editorial on forearm
support and mouse design for computer users. He praises the study design
used by Conlon et al (2), but is a randomised control trial really the
best way to assess ergonomic aids when there are so many confounders?
Simple observation of a group of computer users will identify a range of
postures, as well as a wide variation in arm length...
I welcome the caution shown by Amick (1) in his editorial on forearm
support and mouse design for computer users. He praises the study design
used by Conlon et al (2), but is a randomised control trial really the
best way to assess ergonomic aids when there are so many confounders?
Simple observation of a group of computer users will identify a range of
postures, as well as a wide variation in arm length, wrist diameter, hand
size etc. etc.. I have seen individuals who have undoubtedly benefitted
from ergonomic adjustments to workstations, however the adjustments have
been different in each case. I have seen similar numbers of individuals
harmed by ‘ergonomic supports’ who responded rapidly once the desk was
cleared of squidgy pads.
Consider another aid; we know that safety boots have a key part to
play in reducing injuries, but we do not advocate issuing size 12 boots of
one design to all. Not only should we ensure the boot fits, but some
individuals will just not suit some designs. A randomised control trial
of size 12 boots in a normal workforce may well show that safety boots
cause slips, trips and falls and foot pain (because they don’t fit) rather
than save feet (because they have a steel toe-cap). The same will
inevitably apply to pointing devices and keyboards combined with desk size
and height, chair design and position of equipment; some individuals will
just happen to be ill-suited to the one design bulk-purchased for the
department, while many individuals will be fine with the £25 chair and £5
keyboard and mouse from the discount catalogue.
Similar problems seem to arise with ergonomic assessments such as
those undertaken by Access to Work and others. I have seen too many
reports recommending the same standard ‘ergonomic aids’ for widely
differing conditions (such as pneumatically adjustable chairs for visual
difficulties and wrist extensor tendinitis) to have much faith in any
ergonomic assessment that is based on ‘standard evidence’.
Evidence clearly shows that some individuals get problems, others
don’t. Rather than trying to identify a single solution, should we focus
more on analysing the problem, considering the ‘causal pathway’ as Amick
suggests, but for individuals not populations? Then we can consider the
best individual solution. This means that the issue is not one that
should be based on research evidence, but on the observations of the
occupational physician or nurse on the ground, on clinical assessment and
clinical judgement. This may be a case where ‘more research is not
needed’ unless it is much more clearly focussed; it may just muddy the
waters. Instead we should have two messages:
1. If it ain’t broke, don’t fix it.
2. Assess and intervene early with a tailored solution when problems
do arise.
Tony Williams
(1) Amick BC. Growing knowledge about ‘what works’ to prevent work
injuries. Occupational and Environmental Medicine 2008;65:297-8
(2) Conlon C et al. A randomised controlled trial evaluating an
alternative mouse and forearm support on upper extremity body discomfort
and musculoskeletal disorders among engineers. Occupational and
Environmental Medicine 2008;65:311-18.
As pointed out by the authors, the ultimate carcinogen in the
occupational wood dust exposure is not known. It has been known that
hardwood dust particles are much more harmful than those from softwood
sources. Tannins are versatile markers for hardwood species (1) and their
presence e.g. in the nasal lavage liquid can be used to quantitatively
monitor the dust burden at the target site (2).
As pointed out by the authors, the ultimate carcinogen in the
occupational wood dust exposure is not known. It has been known that
hardwood dust particles are much more harmful than those from softwood
sources. Tannins are versatile markers for hardwood species (1) and their
presence e.g. in the nasal lavage liquid can be used to quantitatively
monitor the dust burden at the target site (2).
Shoemakers are another occupational group in an elevated risk for
sinonasal adenocarcinoma. The common factor could be the use of plant
tannins in the leather treatment. The leather dust tannin content in 24
shops in Lausanne corresponded to that of cherry tree dust (1).
1 Bianco MA, Savolainen H. Woodworkers´ exposure to tannins. J Appl
Toxicol. 1994; 14: 293-295.
2 Mämmelä P, Tuomainen A, Vartiainen T, et al. Biological monitoring
of wood dust exposure in nasal lavage by high-performance liquid
chromatography. J Environ Monit. 2002; 4: 187-189.
To the Editor of Occupational and Environmental Medicine:
We agree with suggestion of Dr. Sjögren that examination of the
exposure-response relationship between occupational exposures and
ischaemic heart disease (IHD) is scientifically justified and is of great
importance to public health. An important motive for exploring this
research question in the work environment are repeated observations in
outdoor pollu...
To the Editor of Occupational and Environmental Medicine:
We agree with suggestion of Dr. Sjögren that examination of the
exposure-response relationship between occupational exposures and
ischaemic heart disease (IHD) is scientifically justified and is of great
importance to public health. An important motive for exploring this
research question in the work environment are repeated observations in
outdoor pollution studies which show elevated risks for cardiovascular
disease in association with exposure to (ultra-) fine particulate matter.
Therefore, the readers may wish to learn that, while examining the
association between occupational exposure to polycyclic aromatic
hydrocarbons (PAH) in road paving and risk of death from IHD, we observed
and reported positive exposure-response association at air concentrations
that may well be typical of polluted urban air[1]. Specifically, there
were 418 cases of fatal IHD in a cohort of 12,367 male asphalt paving
workers from Denmark, Finland, France, Germany, Israel, The Netherlands
and Norway. Both cumulative and average exposure indices for
benzo(a)pyrene (chosen marker of exposure to PAH) were positively and
strongly associated with mortality from IHD. The highest relative risk for
fatal IHD was observed for average benzo(a)pyrene exposures of 273 ng/m3
or higher, for which the relative risk was 1.64 (95% confidence interval
1.13–2.38). External adjustment for potential confounding by smoking
suggested that such confounding was an unlikely explanation for the
result. In the same cohort, we also observed that there was a dose-
response in the association between mortality from obstructive lung
disease (chromic obstructive pulmonary disease and/or asthma combined) and
exposure to PAH[2]. Thus, there may well be mounting evidence that
occupational (and environmental) carcinogens and/or fine particles
resulting from condensation of semi-volatile organic fumes, can cause
certain non-malignant chronic conditions, which is not very surprising
given that tobacco smoke is a recognized cause of a broad range for both
malignant and non-malignant diseases.
Igor Burstyn, PhD
Associate Professor, Community and Occupational Medicine Program,
Department of Medicine, Faculty of Medicine and Dentistry, The University
of Alberta, Edmonton, Canada
iburstyn@ualberta.ca
and
Dick Heederik, PhD
Professor of Health Risk Analysis and Head Division Environmental
Epidemiology
Institute for Risk Assessment Sciences, University Utrecht, Utrecht, The
Netherlands
d.heederik@uu.nl
References
1.Burstyn I, Kromhout H, Partanen T, et al. Polycyclic aromatic
hydrocarbons and fatal ischemic heart disease. Epidemiology 2005;16
(6):744-50.
2. Burstyn I, Boffetta P, Heederik D, et al. Mortality from
Obstructive Lung Diseases and Exposure to Polycyclic Aromatic Hydrocarbons
among Asphalt Workers. Am J Epidemiol 2003;158 (5):468-78.
I am writing to comment on the paper[1] by Morgenstern et al. entitled “Respiratory health and individual estimated exposure to traffic-related air pollutants in a cohort of young children” The paper looked at the health effects of various components of air pollution as they depended on distance from major traffic arteries in and around Munich, Germany. I do not disagree with the data of that paper, which was obtained in a hig...
I am writing to comment on the paper[1] by Morgenstern et al. entitled “Respiratory health and individual estimated exposure to traffic-related air pollutants in a cohort of young children” The paper looked at the health effects of various components of air pollution as they depended on distance from major traffic arteries in and around Munich, Germany. I do not disagree with the data of that paper, which was obtained in a highly competent fashion. Rather, I want to suggest a novel hypothesis that might help to explain the results.
The key finding I want to examine is the observed association of ambient NO2 levels and nocturnal cough in very young children.
Morgenstern’s Table 4 shows that NO2 concentrations (a misprint in the units) varied from 19.4 to 71.7 ìg/m3, with a mean of 35.4. Those concentrations are much lower than those that have been demonstrated to have harmful effects, at least in adults. According to one authoritative review[2] there is little evidence that NO2 has any respiratory effect, even on asthmatics, at concentrations less than 200 ppb (376 ìg/m3 ).
An excellent review[3] of the health effects of outdoor NO2 concluded:. “The overall results suggest that outdoor NO2 was serving as a marker for more causal agents ...” That conclusion obviously suggests that there may be a missing (unknown) pollutant that can, in some circumstances, mimic NO2 in ecological studies. Other environmental epidemiologists have expressed the suspicion that some effects associated with criterion pollutants may instead be due to unmeasured confounding pollutants[4]. One paper[5] specifically suggested that the observed association of children’s symptoms with NO2 could mean that the NO2 was a marker for other components of vehicular exhaust.
The idea that NO2 may have harmful effects on young children is not new. However, the existing literature could be described as conflicting[6], with one study[7] of indoor NO2 at concentrations in the range 60-300 ìg/m3 finding no effect in children aged 6-9 years. I found several papers that found no such association, including four that looked at infants[8-11]. These results make it unlikely that NO2 itself was the direct cause of the cough.
Since the cough was seen only at night, we should think of a pollutant whose concentrations are larger at night than in daytime. We are not aware of any diurnal data on NO2 in Munich. However, studies in California[12 13], Finland[14], Stuttgart[15], and Rome[16] indicate that daytime concentrations are generally larger than those seen late at night. That result is comprehensible for two reasons: (1) In most cities traffic density is much less at night than in daytime, and (2) the production of NO2 from NO is greatly accelerated by ozone in the air, which is maximal in daytime. I know of no urban study indicating that NO2 is primarily a nocturnal pollutant.
For several years I have argued that methyl nitrite (MN) is an important but unrecognized exhaust component of engines with methyl ether (such as MTBE) in the fuel[17]. MN has the very unusual property that it is rapidly destroyed by photolysis from sunlight[18]. Photolysis[19 20] of MN produces NO, which is naturally oxidized to NO2 by sunlight. These facts have two immediate consequences: (1) on most (sunny) days MN will be a strictly nocturnal pollutant, and (2) on sunny mornings NO2 will be a marker for MN of the previous night. MN is stable in night air[21]. Hence MN has exactly the properties that might explain the apparent association of NO2 with nocturnal cough.
Readers wishing to learn more about MN might want to read my recent paper[22]entitled “Paradoxical Ozone Associations could be due to Methyl Nitrite from Combustion of Methyl Ethers or Esters in Engine Fuels”. That paper focused on several ozone studies that, inexplicably, found negative associations of ozone with morbidity, especially for asthma in children[23 24]. I argued that MN has exactly the properties needed to explain those associations, and may also explain a large part of the increase in asthma prevalence seen in the US over the period 1980-2000.
I want to thank Dr. Joachim Heinrich for recently bringing the Morgenstern paper to my attention.
References
1. Morgenstern V, Zutavern A, Cyrys J, Brockow I, Gehring U, Koletzko S, et al. Respiratory health and individual estimated exposure to traffic-related air pollutants in a cohort of young children.[see comment]. Occupational & Environmental Medicine 2007;64(1):8-16.
2. Committee. Health effects of outdoor air pollution. Part 2. Committee of the Environmental and Occupational Health Assembly of the American Thoracic Society. American Journal of Respiratory & Critical Care Medicine 1996;153(2):477-98.
3. Delfino RJ. Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research. Environ Health Perspect 2002;110 Suppl 4:573-89.
4. Janes H, Dominici F, Zeger SL. Trends in air pollution and mortality - An approach to the assessment of unmeasured confounding. Epidemiology 2007;18(4):416-423.
5. Salome CM, Brown NJ, Marks GB, Woolcock AJ, Johnson GM, Nancarrow PC, et al. Effect of nitrogen dioxide and other combustion products on asthmatic subjects in a home-like environment. European Respiratory Journal 1996;9(5):910-8.
6. Samet JM, Utell MJ. The risk of nitrogen dioxide: what have we learned from epidemiological and clinical studies? Toxicology & Industrial Health 1990;6(2):247-62.
7. Brunekreef B, Houthuijs D, Dijkstra L, Boleij JSM. Indoor Nitrogen-Dioxide Exposure and Childrens Pulmonary-Function. Journal of the Air & Waste Management Association 1990;40(9):1252-1256.
8. Sunyer J, Puig C, Torrent M, Garcia-Algar O, Calico I, Munoz-Ortiz L, et al. Nitrogen dioxide is not associated with respiratory infection during the first year of life. International Journal of Epidemiology 2004;33(1):116-20.
9. Farrow A, Greenwood R, Preece S, Golding J. Nitrogen dioxide, the oxides of nitrogen, and infants' health symptoms. ALSPAC Study Team. Avon Longitudinal Study of Pregnancy and Childhood. Archives of Environmental Health 1997;52(3):189-94.
10. Baker RJ, Hertz-Picciotto I, Dostal M, Keller JA, Nozicka J, Kotesovec F, et al. Coal home heating and environmental tobacco smoke in relation to lower respiratory illness in Czech children, from birth to 3 years of age. Environmental Health Perspectives 2006;114(7):1126-32.
11. Samet JM, Lambert WE, Skipper BJ, Cushing AH, Hunt WC, Young SA, et al. Nitrogen dioxide and respiratory illnesses in infants. American Review of Respiratory Disease 1993;148(5):1258-65.
12. Grosjean D. Distribution of Atmospheric Nitrogenous Pollutants at a Los-Angeles Area Smog Receptor-Site. Environmental Science & Technology 1983;17(1):13-19.
13. Horie Y, Mirabella V. Estimating Future NO2 Levels in the Greater Los-Angeles Area by Source-Type Contribution. Journal of the Air Pollution Control Association 1982;32(3):266-273.
14. Vakeva M, Hameri K, Kulmala M, Lahdes R, Ruuskanen J, Laitinen T. Street level versus rooftop concentrations of submicron aerosol particles and gaseous pollutants in an urban street canyon. Atmospheric Environment 1999;33(9):1385-1397.
15. Mayer H. Air pollution in cities. Atmospheric Environment 1999;33(24-25):4029-4037.
16. Gariazzo C, Silibello C, Finardi S, Radice P, Piersanti A, Calori G, et al. A gas/aerosol air pollutants study over the urban area of Rome using a comprehensive chemical transport model. Atmospheric Environment 2007;41(34):7286-7303.
17. Evidence for methyl nitrite as an exhaust component from engines with certain fuels. Annual Meeting Proceedings CD-ROM Air & Waste Management Association, 99th, New Orleans, LA, June 20-23, 2006; 2006; New Orleans, LA.
18. Seinfeld JH, Pandis SN. Atmospheric chemistry and physics : from air pollution to climate change. New York: Wiley, 1998.
19. Zhao WX, Gao XM, Hao LQ, Huang MQ, Huang T, Wu T, et al. Use of integrated cavity output spectroscopy for studying gas phase chemistry in a smog chamber: Characterizing the photolysis of methyl nitrite (CH3ONO). Vibrational Spectroscopy 2007;44(2):388-393.
20. Bruhlmann U, Dubs M, Huber JR. Photodissociation of Methylnitrite - State Distributions, Recoil Velocity Distribution, and Alignment Effects of the NO (X2-Pi) Photofragment. Journal of Chemical Physics 1987;86(3):1249-1257.
21. Goss LM, Mortensen CD, Blake TA. Rotationally resolved spectroscopy of the õ8 band of cis-methyl nitrite. Journal of Molecular Spectroscopy 2004;225(2):182-188.
22. Joseph PM. Paradoxical ozone associations could be due to methyl nitrite from combustion of methyl ethers or esters in engine fuels. Environment International 2007;33:1090-1106.
23. Buchdahl R, Parker A, Stebbings T, Babiker A. Association between air pollution and acute childhood wheezy episodes: prospective observational study. Bmj 1996;312(7032):661-5.
24. Buchdahl R, Willems CD, Vander M, Babiker A. Associations between ambient ozone, hydrocarbons, and childhood wheezy episodes: a prospective observational study in south east London. Occup Environ Med 2000;57(2):86-93.
In their recent article (1), Mary Schubauer-Berigan and colleagues
elaborate on a prior study (2) in order to examine potential confounding
by birth cohort and hire age of the relationship between beryllium
exposure and lung cancer, a worthwhile objective. The prior study is a
matched nested case-control study that employs incidence density sampling
to match controls to cases and uses exposure lag...
In their recent article (1), Mary Schubauer-Berigan and colleagues
elaborate on a prior study (2) in order to examine potential confounding
by birth cohort and hire age of the relationship between beryllium
exposure and lung cancer, a worthwhile objective. The prior study is a
matched nested case-control study that employs incidence density sampling
to match controls to cases and uses exposure lagging to take disease
latency into consideration. However, its study design is unable to
distinguish between null and alternate hypotheses owing to artifacts
caused by imbalances in the matching of controls to cases on age of
censor. These artifacts result in case-control differences in hire age and
date of birth as well as in controls having an artificially high rate of
truncated lagged exposure when compared to cases. This sequence of
measurement error, in turn, produces artificially high lagged exposure
odds ratios (3,4,5).
Our simulations (unpublished) demonstrate that these study design
artifacts are not completely reversed through analysis, for instance, by
simply adding hire age to a conditional logistic regression model. An
alternative approach is required, such as closer matching of cases and
controls on age at censor (4). The current study (1) inherits the
artifacts present in the prior study (2), as it uses the same cases,
differentially matched controls, and calculation of artifacts in lagged
exposure, with minor changes in the method for substituting small values
for zero. The authors have not shown that the current study design
eliminates or controls the inherent artifacts or that it corrects the
inability of the prior study design to distinguish null and alternative
hypotheses.
1) Schubauer-Berigan MK, Deddens JA, Steenland K et al. Adjustment
for temporal confounders in a reanalysis of a case-control study of
beryllium and lung cancer. Occup Environ Med doi:10.1136/oem.2007.033654.
2) Sanderson WT, Ward EM, Steenland L et al. Lung cancer case-control
study of beryllium workers. Am J Ind Med 2001; 39:133-144.
3) Deubner DC, Roth HD, Levy PS. Empirical evaluation of complex
study designs: workplace exposure and cancer. J Occup Environ Med 2007,
49:953-959.
4) Levy PS, Roth HD, Deubner DC. Exposure to beryllium and occurrence
of lung cancer: a reexamination of findings from a nested case-control
study. J Occup Environ Med 2007, 49:96-101
5) Levy P.S., Deubner D.C. and Levy P.S., Authors’ response to letter
to the editor. J Occup Environ Med 2007, 49:707-711
Sincerely,
David C. Deubner
H. Daniel Roth
Paul S. Levy
David C. Deubner is an employee of Brush Wellman Inc, a manufacturer
of beryllium materials
H. Daniel Roth (Roth Associates, Rockville, Maryland, USA) and Paul
S. Levy (Research Triangle Institute International, Research Triangle
Park, North Carolina, USA) are supported in part through contracts, direct
and indirect, with Brush Wellman Inc.
We thank Markku Seuri and Jukka Uitti for their interest towards our
article [1] and for raising the topics for discussion in OEM (eLetter
posted 16 October).
Concerning the first topic, the intervention in the RCT1 among the
High Risk subjects consisted of 1) personal feedback of the health survey
results and 2) an invitation to a consultation at their local occupational
health service (OHS). The main purpose...
We thank Markku Seuri and Jukka Uitti for their interest towards our
article [1] and for raising the topics for discussion in OEM (eLetter
posted 16 October).
Concerning the first topic, the intervention in the RCT1 among the
High Risk subjects consisted of 1) personal feedback of the health survey
results and 2) an invitation to a consultation at their local occupational
health service (OHS). The main purpose of the OHS consultation was the
construction of an action plan, and if appropriate, referral to a further
consultation by a specialist or psychologist. Of the subjects in the
intervention group (n = 209), 142 (68%) attended the consultation at OHS.
50 did not attend for unknown reasons. The employment had terminated with
17 subjects during the follow-up. Of the attendees, five refused further
examinations or interventions, and the OHS professionals had considered
that eight subjects did not warrant further actions. Eventually 129
subjects ended up receiving something: health advice (n=106), referral to
consultation or hospital outpatient clinic (n=64), or a group intervention
at the OHS (n=6), in different combinations. As 64 subjects were referred
to specialist treatment, it is reasonable to assume that they had had
clinically significant disorders. Moreover, of the 142 subjects who
visited OHS, 72 (51%) had not received earlier treatment at OHS for the
respective reasons for belonging to the High Risk group. With the health
survey and subsequent invitation to OHS we obviously succeeded in
capturing many workers with underlining health problems that had not been
properly attended to. We discuss this and other possible mechanisms of the
effectiveness in more detail in our recently published paper concerning
the cost-effectiveness of the same intervention [2]. We preferred not to
present the on-treatment subgroup analysis, as it was not stated in our
study protocol. However, we have done the analysis: among those 50
subjects that did not attend the intervention sickness absence tended to
increase from 18 days to 25 days, while among those who attended the
intervention sickness absence days at baseline and follow up were the
same, 17 days. This provides further support to the view that the targeted
OHS intervention was indeed accountable for the effectiveness rather than
the feedback letter.
As regards the second point we are somewhat confused. We do not write
about “the reduction of sickness absence in the intervention group” in the
article. As we present in the results, the mean, median and total sickness
absence days increased, and the proportion of subjects with zero absence
decreased in the control group. No change took place in the mean, median
and total sickness absence days, or in the proportion of subjects with
zero absence in the intervention group. Based on this we concluded that
the OHS intervention was effective in controlling work loss. Nothing very
extraordinary happened in the company either: the mean of sickness absence
days in the study cohort increased from 10 to 12 days (i.e., one per cent
unit) and the increase mainly took place in the control group arm in the
High Risk group: the increases were 0.2, 0.7 and 2.6 per cent units in the
Low Risk, Intermediate Risk and High Risk groups, respectively. The
increase in sickness absence in this specific company did not differ from
the industry sector. However, as we write in our paper [1], future
research should address the question of whether the same intervention
approach is effective in different occupational settings and professional
groups.
The evidence on effectiveness of interventions undertaken by occupational
health care units in reducing sickness absence among high risk employees
is meager. We do hope that our randomized controlled trial will encourage
occupational health clinicians and scientists to undertake randomized
trials and increase the evidence base of the field.
1 Taimela S, Malmivaara A, Justen S. et al. The effectiveness of two
occupational health intervention programs in reducing sickness absence
among employees at risk. Two randomised controlled trials. Occup Environ
Med published online 6 Aug 2007;doi10.1136/oem.2007.032706.
2 Taimela S, Justen S, Aronen P. et al. An occupational health
intervention program for workers at high risk for sickness absence. Cost-
effectiveness analysis based on a randomised controlled trial. Occup
Environ Med published online 12 Oct 2007 doi:10.1136/oem.2007.033167
The work by Kivimäki et al (64:659-665) is part of an important
tradition that aims to expand understanding of occupational psychosocial
stressors to include issues of justice and fairness in the workplace,
complementing the two most well-known models, demand-control and effort-
reward. We applaud this work, while we also agree with the commentary by
Renée Bourbonnais (64:640-641) that the existing conceptual frameworks...
The work by Kivimäki et al (64:659-665) is part of an important
tradition that aims to expand understanding of occupational psychosocial
stressors to include issues of justice and fairness in the workplace,
complementing the two most well-known models, demand-control and effort-
reward. We applaud this work, while we also agree with the commentary by
Renée Bourbonnais (64:640-641) that the existing conceptual frameworks for
identifying job stressors are simultaneously overlapping and incomplete.
Further, we echo her point that the conceptual basis of relational justice
needs to be more fully examined to clarify how it goes beyond existing
models – since, as Kivimäki and coworkers acknowledge, the concept of
equity is related to but not totally subsumed under the construct of
effort-reward imbalance. We also believe that apparent unavailability of
measures to examine workplace injustice has delayed examination of its
importance for mental and other health outcomes.
Discriminatory treatment within the workplace is a clear example of
injustice that negatively impacts the three dimensions of self esteem,
self-efficacy, and belonging cited by Bourbonnais. The current focus on
procedural and relational injustice is perhaps not so much new as a
reframing, in that there is already a substantial literature addressing
the adverse health effects of gender and racial discrimination. For
example, racism in the United States has been documented to have negative
associations with psychological well-being [1-5] and physical health [5-9]
and is increasingly recognized as accounting directly for some of the
differences in psychological and physical health between whites and people
of color [9-13]. For example, a thirteen-year panel study conducted by
Jackson and colleagues [5] demonstrated that racial discrimination
affected both the physical and mental health of African Americans. Krieger
and Sidney [6] showed that experiences of racial discrimination, as well
as acceptance of unfair treatment as inevitable, were associated with
higher levels of blood pressure in African American participants.
The literature is still rather sparse on the specific health effects
of racial discrimination in the work environment. Mays and co-workers
[14] reported that perceived race-based discrimination in the labor market
affected advancement, skill development, and interpersonal relationships
with coworkers among African American women. Similarly, Hughes and Dodge
[15] found that both interpersonal and institutional racism at work,
especially interpersonal prejudice, were significant predictors of job
satisfaction.
With regard to gender issues, sexist treatment of women at work –
discrimination, negative sex stereotyping, isolation and sexual
objectification - has been associated with adverse mental and physical
health conditions, including high blood pressure, ulcers, tension, and
insomnia [16-18]. Women who reported gender discrimination in their
workplace also had lower levels of job satisfaction and organizational
commitment, as well as more negative relations with coworkers and
supervisors [19-21]. The effects of sexual harassment at work are
similar: negative psychological outcomes such as anxiety, depression,
alienation, and lower self-esteem [22-24]; smoking and alcohol abuse [25];
and negative somatic outcomes such as gastrointestinal disturbances,
headache, and insomnia [16, 26-29].
While we agree with Bourbonnais that the pathways through which
organizational practices are linked to individual health outcomes are not
clear, we would argue that organizational issues are indeed important to
explore. Like the other models of job stress, workplace discrimination
can be defined both at the level of the organization and at the level of
the individual, and these are clearly correlated with each other. For
example, the frequency of sexual harassment behavior by individuals has
been shown to be higher in work climates where sexist stereotypes and
attitudes are tolerated [21, 30-32] and where an organization is
unresponsive to employee concerns and complaints [20, 28]. Furthermore,
experiences of discrimination are distributed differentially by
socioeconomic position [33]. Incidents of injustice affect not only those
immediately targeted; even sexual harassment directed at someone else in
the workplace can cause lower job satisfaction, job withdrawal,
psychological distress and somatization [34]. Additionally, job
segregation plays a role as women and people of color are often relegated
to jobs with less control, high stress, and low influence [35], which then
translates into poor health outcomes [36]. Interestingly, we found that
perceived sexism in an academic workplace was associated with lower job
satisfaction for women and men [19].
It is unfortunate that time pressure and disciplinary gaps tend to
keep researchers unaware of relevant research methods and findings in
fields other than our own that could expand our understanding of the
impact of equity at work. With an eye to rectifying this omission, and
with the support of the U.S. National Institute for Occupational Safety
and Health, we have recently compiled a large set of survey measures on
sex and race discrimination, sexual harassment, and work-family balance,
with detailed examination of the psychometric properties of each one.
Most of these measures were found in the psychology literature, but it is
our hope that occupational health researchers will now have easier access
to them and thus will broaden their investigations of job stress. This
measures compendium will be forthcoming this fall from NIOSH [37].
References
1. Harrell SP. Researching racism and psychological well-being:
Conceptualization and change. 105th Convention of the American
Psychological Association; 1997; Chicago, IL; 1997.
2. Klonoff EA, Landrine, H., & Ullman, J.B. . Racial
discrimination and psychiatric symptoms among blacks. Cultural Diversity
Ethnic Minority Psych 1999;5:329-39.
3. Neighbors HW, Jackson JS, Broman CL, et al. Racism and the mental
health of African Americans: The role of self and system blame. Health
Ethnicity Dis 1996;6:167-75.
4. Utsey SO, Ponterotto JG. Development and validation of the index
of race-related stress (IRRS). J Counseling Psych 1996;43:490-501.
5. Jackson JS, Brown TN, Williams DR, et al. Racism and the physical
and mental health status of African Americans: A thirteen year national
panel study. Health Ethnicity Dis 1996;6:132-47.
6. Krieger N, Sidney S. Racial discrimination and blood pressure:
The CARDIA study of young black and white adults. Amer J Pub Health
1996;86:1370-8.
7. Krieger N. Does racism harm health? Did child abuse exist before
1962? On explicit questions, critical science and current controversies:
An ecosocial perspective. Amer J Pub Health 2003;93:194-9.
8. Rowley DL. Research issues in the study of very low birthweight
and preterm delivery among African Americans. J National Med Assoc
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Cherrie et al, in response to McDonald et al's recent gas mask worker analysis [1], have suggested using a crocidolite fibre clearance half-life of 20 years. In their analyses, McDonald et al used a half-life of 10 years [1].
The best figure to use might be a half-life of 92 months, as estimated previously [2].
1. McDonald JC, Harris JM, Berry G. Sixty years on: the price of assembling military gas masks in 1940. Occup Environ...
Cherrie et al, in response to McDonald et al's recent gas mask worker analysis [1], have suggested using a crocidolite fibre clearance half-life of 20 years. In their analyses, McDonald et al used a half-life of 10 years [1].
The best figure to use might be a half-life of 92 months, as estimated previously [2].
1. McDonald JC, Harris JM, Berry G. Sixty years on: the price of assembling military gas masks in 1940. Occup Environ Med. 2006; 63: 852-5.
2. de Klerk NH, Musk AW, Williams VM, Filion PR, Whitaker D, Shilkin KB. Comparison of measures of exposure to asbestos in former crocidolite workers from Wittenoom Gorge, W. Australia. Am J Ind Med 1996;30:579-587.
I commend Steenstra et al (2005) for their paper and its succinct
systematic review of quality inception cohorts in the area of acute low
back pain (ALBP). Many of the 79 items discussed have been long overdue
such a review and I was quite surprised to learn that many traditional
practice patterns (e.g. asking ALBP patients about smoking status,
previous LBP history) might need some reconsideration...
I commend Steenstra et al (2005) for their paper and its succinct
systematic review of quality inception cohorts in the area of acute low
back pain (ALBP). Many of the 79 items discussed have been long overdue
such a review and I was quite surprised to learn that many traditional
practice patterns (e.g. asking ALBP patients about smoking status,
previous LBP history) might need some reconsideration so far as how we
think they influence sick leave.
Having used this paper as part of a literature review for part fulfillment
of my MSc, I must alert other readers to the confusing referencing
contained within this paper. Specifically pp. 855 is one such example
where para 5 commences "Two high quality studies reported social
dysfunction [24] and social isolation [35 36]..." References 35 & 36
are clearly two different papers and one isn't clear as to which HQ paper
the author is referring to! Indeed two citations appear in the superscript
yet the text alludes to a singular. This "bundling" of reference citations
occurs many times throughout the review and makes independent review &
retrieval of the papers needlessly difficult.
Small omissions are noted also in declaring race and income as non-
significant yet the pooled effect sizes (ES) are not declared in the table
with other items. I also believe there is an error in declaring lack of
energy not significant when the ES in Table 5 seems significant.
I believe this paper helps researchers identify methodological issues with
such complex research and proves a useful summary of key factors in sick
leave. I am not sure however that many of us could include "all"
prognostic factors when doing actual research. I would very much like to
have gained some insight into why they selected the final 15 "promising
factors for further research". Again lack of energy appears incongrously
given the earlier assertions.
Taimela et al published the results of two RCTs 1. Trials are validly
conducted, but two points need further consideration.
Firstly, one should ask what was the effective intervention. Occupational
health carried out three actions. Firstly they identified the high-risk
employees, secondly they sent a letter of the intervention program only to
those in the intervention group and thirdly consultations were given to
those wil...
Taimela et al published the results of two RCTs 1. Trials are validly
conducted, but two points need further consideration.
Firstly, one should ask what was the effective intervention. Occupational
health carried out three actions. Firstly they identified the high-risk
employees, secondly they sent a letter of the intervention program only to
those in the intervention group and thirdly consultations were given to
those willing to participate (participation rate only 68%). The
consultations led health advice, consultation or group intervention. The
analysis was conducted according to the principle of intended to treat. No
results concerning those actually treated were given. The effective
treatment was not necessarily what the occupational health did with the
patients but the letter that was sent only to the intervention group. This
letter obviously increased personal consciousness of the high-risk
behaviour and may by itself act as intervention for the observed change.
More information about the effective action would have been available if
the results were given by the principle of actually treated.
Secondly, the authors write about “the reduction of sickness absence” in
the intervention group. This is not quite so, since the mean number of
sickness absence days at baseline was 19.7 per year and 19.3 during the
follow-up. This is not a reduction. However, the number of sickness
absence days increased in the control group from 17.9 to 29.9 days per
year and in the study population at large from 18.8 to 24.6 days per year.
At the same time the general increase in sickness absence in Finland grew
only less than 0.5 per cent. Something very extraordinary happened in the
studied company and that leads one to ask how well the results can be
applied in companies of stabile level of absenteeism.
1 Taimela S, Malmivaara A, Justen S. et al. The effectiveness of two
occupational health intervention programs in reducing sickness absence
among employees at risk. Two randomised controlled trials. Occup Environ
Med published online 6 Aug 2007;doi10.1136/oem.2007.032706.
Sir
I welcome the caution shown by Amick (1) in his editorial on forearm support and mouse design for computer users. He praises the study design used by Conlon et al (2), but is a randomised control trial really the best way to assess ergonomic aids when there are so many confounders? Simple observation of a group of computer users will identify a range of postures, as well as a wide variation in arm length...
Dear Editor,
As pointed out by the authors, the ultimate carcinogen in the occupational wood dust exposure is not known. It has been known that hardwood dust particles are much more harmful than those from softwood sources. Tannins are versatile markers for hardwood species (1) and their presence e.g. in the nasal lavage liquid can be used to quantitatively monitor the dust burden at the target site (2).
...To the Editor of Occupational and Environmental Medicine:
We agree with suggestion of Dr. Sjögren that examination of the exposure-response relationship between occupational exposures and ischaemic heart disease (IHD) is scientifically justified and is of great importance to public health. An important motive for exploring this research question in the work environment are repeated observations in outdoor pollu...
To the editor
In their recent article (1), Mary Schubauer-Berigan and colleagues elaborate on a prior study (2) in order to examine potential confounding by birth cohort and hire age of the relationship between beryllium exposure and lung cancer, a worthwhile objective. The prior study is a matched nested case-control study that employs incidence density sampling to match controls to cases and uses exposure lag...
We thank Markku Seuri and Jukka Uitti for their interest towards our article [1] and for raising the topics for discussion in OEM (eLetter posted 16 October).
Concerning the first topic, the intervention in the RCT1 among the High Risk subjects consisted of 1) personal feedback of the health survey results and 2) an invitation to a consultation at their local occupational health service (OHS). The main purpose...
The work by Kivimäki et al (64:659-665) is part of an important tradition that aims to expand understanding of occupational psychosocial stressors to include issues of justice and fairness in the workplace, complementing the two most well-known models, demand-control and effort- reward. We applaud this work, while we also agree with the commentary by Renée Bourbonnais (64:640-641) that the existing conceptual frameworks...
Dear Editor,
I commend Steenstra et al (2005) for their paper and its succinct systematic review of quality inception cohorts in the area of acute low back pain (ALBP). Many of the 79 items discussed have been long overdue such a review and I was quite surprised to learn that many traditional practice patterns (e.g. asking ALBP patients about smoking status, previous LBP history) might need some reconsideration...
Taimela et al published the results of two RCTs 1. Trials are validly conducted, but two points need further consideration. Firstly, one should ask what was the effective intervention. Occupational health carried out three actions. Firstly they identified the high-risk employees, secondly they sent a letter of the intervention program only to those in the intervention group and thirdly consultations were given to those wil...
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