Firstly, latent period always refers to the period between the point
of the time when disease occurs and point of the time when the disease is
detected, while tumour induction time refers to the period between the
point of the time when the component cause (can be an exposure) is
satisfied and the point of the time when the disease is occurred.[1]
Thus only under the extreme condition that one
secon...
Firstly, latent period always refers to the period between the point
of the time when disease occurs and point of the time when the disease is
detected, while tumour induction time refers to the period between the
point of the time when the component cause (can be an exposure) is
satisfied and the point of the time when the disease is occurred.[1]
Thus only under the extreme condition that one
second of mobile use may cause brain tumours, while once the tumour is
‘born’, it can be detected, it would be possible to defined the latency
period as the period between ‘first use of a cellular or cordless
telephone until tumour diagnosis’.
Secondly, in the research exposure to ‘microwaves’ is classified as a
chronic exposure (such as smoking) rather than a point exposure (such as
exposure to toxic gas for one minute). While the exposure is measured by
the total hours use of different types mobile, and they compared the
effect of different exposure dose (lower or above 85 hours) under
different length of ‘latency period’. However the effect of certain dose
of exposure will only appear after the subjects already exposed to that
dose of exposure. For example, the effect of exposure to 85 hours of digital
mobile use on the incident of brain tumours, might only possibly appear
after the subjects has already been exposed to 85 hours of digital mobile use.
Similarly, it is unrealistic to measure the effect of exposure to 10 pack-
year smoking on risk of lung cancer, since the first day when the subjects
pick up their first cigarettes.
Furthermore, there may be subjects who use more than one kind of the
mobile that have been listed in the article, effect of multiple exposures
have not been measured in the research.
In addition people with ‘Zero’ exposure may not be a good comparison.
People who never use mobile may be rare in today’s society, as to say even
control for gender, age, socio-economic status, they may still have
special characters different from people who use mobile such as smoking,
alcohol use, diet habit, physical activity etc. Above all, exposure is always extremely hard to measure validly, and sometimes it may even hard to define, however these are always essential
for the accuracy of a study.
Reference
1. Rothman, J. & Greenland, S. Modern Epidemiology, 1998, Lippincott-Raven.
The paper by Nicholson et al. provides useful evidence-based
guidelines for prevention, identification, and management of occupational
asthma (OA) based on a comprehensive review of the literature.[1]
Evidence statements 6 and 7 list the workers most commonly reported to OA
surveillance schemes or reported from population studies to be at
increased risk of developing asthma. Hairdressers are n...
The paper by Nicholson et al. provides useful evidence-based
guidelines for prevention, identification, and management of occupational
asthma (OA) based on a comprehensive review of the literature.[1]
Evidence statements 6 and 7 list the workers most commonly reported to OA
surveillance schemes or reported from population studies to be at
increased risk of developing asthma. Hairdressers are not included in
these lists, but we believe that they should be.
Data from the French national OA surveillance programme (ONAP) show that
hairdressing represents the fourth most frequent occupation (both sexes)
and the second most frequent occupation in women, among subjects with OA.[2]
According to this programme, the annual incidence rate was 308 per
million in hairdressers, whereas the mean annual incidence of OA in France
was estimated to be 24 cases per million workers. In Sweden, the self-
reported rate of OA in female hairdressers was 129 per million, whereas
the annual crude reporting rate for women was 70 per million.[3]
Several population-based studies have also shown an increased risk of OA
in hairdressers. In Finland, the risk of OA was significantly increased in
hairdressers, both in men (RR: 2.09; 95%CI: 1.12-3.89) and in women (RR:
1.61; 95%CI: 1.45-1.79), using a reference group with little exposure to
dusts, fumes, vapours, or other workplace air-pollution.[4] In Spain, an
increased risk of asthma, defined by the presence of wheezing or whistling
in the chest during the previous 12 months, was observed in hairdressers,
but was not statistically significant (OR: 1.94; 95%CI: 0.86-4.39).[5]
These data are also consistent with the results of a Swedish nationwide
retrospective study showing a moderately increased asthma risk among non-
smoking hairdressers [6], and with the results of a Finnish retrospective
cohort study using a self-administered questionnaire showing a relative
risk for developing asthma of 1.7 (95%CI: 1.1-2.5) among hairdressers,
compared with referents.[7]
References
1. Nicholson PJ, Cullinan P, Taylor AJ, Burge PS, Boyle C.
Evidence based guidelines for the prevention, identification, and
management of occupational asthma. Occup Environ Med 2005;62:290-9.
2. Ameille J, Pauli G, Calastreng-Crinquand A, Vervloet D,
Iwatsubo Y, Popin E et al. Reported incidence of occupational asthma in
France, 1996-99: the ONAP programme. Occup Environ Med. 2003;60:136-41.
3. Toren K. Self reported rate of occupational asthma in Sweden
1990-2. Occup Environ Med 1996;53:757-61.
4. Karjalainen A, Kurppa K, Martikainen R, Karjalainen J, Klaukka
T. Exploration of asthma risk by occupation: extended analysis of an
incidence study of the Finnish population. Scand J Work Environ Health
2002;28:49-57.
5. Kogevinas M, Anto JM, Soriano JB, Tobias A, Burney P. The risk
of asthma attributable to occupational exposures. A population-based study
in Spain. Spanish Group of the European Asthma Study. Am J Respir Crit
Care Med 1996;154:137-43.
6. Albin M, Rylander L, Mikoczy Z, Lillienberg L, Dahlman HA,
Brisman J et al. Incidence of asthma in female Swedish hairdressers. Occup
Environ Med 2002;59:119-23.
7. Leino T, Tammilehto L, Luukkonen R, Nordman H. Self reported
respiratory symptoms and diseases among hairdressers. Occup Environ Med
1997;54:452-5.
The review of occupational asthma by Nicholson et al. [1] is
comprehensive. It is an important report that is likely to be widely
read: the evidence review of low back pain has, for example, been one of
the most commonly downloaded articles [2]. The appearance in the
principal recommendations of the authors’ unsubstantiated opinions is,
therefore, concerning.
The review of occupational asthma by Nicholson et al. [1] is
comprehensive. It is an important report that is likely to be widely
read: the evidence review of low back pain has, for example, been one of
the most commonly downloaded articles [2]. The appearance in the
principal recommendations of the authors’ unsubstantiated opinions is,
therefore, concerning.
The authors also include issues in the principal recommendations that
are not supported by evidence. By including these with others the
appearance is given that evidence exists. They recommend that
"surveillance should include … immunological tests where appropriate" despite an absence of evidence that these tests are of benefit in surveillance. They also recommend that surveillance should be provided
"at least annually". No evidence is provided that surveillance should be
delivered on this basis. I am not aware of any studies comparing
surveillance intervals.
These issues have important implications for the practice of health
surveillance. Applied without thought they could lead to pressure on
employers to provide surveillance that is unnecessarily costly and
frequent. More importantly they could lead to pressure on employees to
accept invasive procedures of questionable or no value in surveillance
that could then have important implications for their employment. I have
noted in this journal on a previous occasion the tendency to interpret
data in a way that reinforces existing opinion to the potential
disadvantage of workers at risk of occupational asthma and their
employers [3].
This additional "expert opinions" complement the evidence review.
However, it would have been better to either distinguish them clearly from
the evidence or make it clearer that there is an absence of evidence to
underpin these opinions.
References
1. Nicholson PJ, Cullinan P, Newman Taylor AJ, et al. Evidence based
guidelines for the prevention, identification, and management of
occupational asthma. Occup Environ Med 2005;62:290–9.
2. Top ten downloads from Occupational Medicine. Occup Med (Lond)
2005;55:74.
3. RM Preece. Lung function decline in laboratory animal workers
[electronic response to Portengen et al. Lung function decline in
laboratory animal workers: the role of sensitisation and exposure]
occenvmed.com 2003 http://oem.bmjjournals.com/cgi/eletters/60/11/870#90.
Timonen and colleagues reported the association between urinary
concentration of lung Clara cell protein CC16, a marker for lung damage,
and daily variation in fine and ultrafine particulate air pollution in
three cities of Netherlands (Amsterdam), Germany (Erfurt), and Finland
(Helsinki). They found that in Amsterdam and Erfurt, there were no
significant association between PM2.5 and concentration...
Timonen and colleagues reported the association between urinary
concentration of lung Clara cell protein CC16, a marker for lung damage,
and daily variation in fine and ultrafine particulate air pollution in
three cities of Netherlands (Amsterdam), Germany (Erfurt), and Finland
(Helsinki). They found that in Amsterdam and Erfurt, there were no
significant association between PM2.5 and concentration of CC16. In
Helsinki, CC16 concentration increased with increasing levels of PM2.5,
especially among male subjects and subjects with lung disorders. They
mentioned that the reason why the effect was observed in Helsinki is not
yet understood [1].
Mutation detection methods identified an adenine to guanine
substitution in the CC16 gene at position 38 (A38G) downstream from the
transcription initiation site within the non-coding region of exon 1. It
is suggested that the 38G allele is more likely to be the wild type and
the 38A allele is the mutant type [2]. Also it is showed that the 38A
sequence was associated with reduced plasma CC16 levels [3]. The gene
encoding CC16 are localized to chromosome 11q13, a region occupied by
several genes involved in the regulation of allergy and inflammation. The
CC16 genetic polymorphism was associated with asthma [2-5]. The 38A allele
showed a frequency about 30 percent in the studied populations and to be
associated with a significantly increased risk of developing asthma [2, 4,
5].
Based on the Table 1 of Timonen et al. report, 19 percent of subjects in
Helsinki had asthma, whereas only about one percent of Amsterdam and
Erfurt subjects suffering from asthma [1]. This difference is highly
significant (2-tailed Fisher’s exact test; P=0.0009). Assuming that the
CC16 genotypes are associated with asthma, it may be say that there is a
significant difference between Helsinki subjects and subjects of both
Amsterdam and Erfurt for CC16 genotypes. It is suggested that the genetic
polymorphism of CC16 in relation to the air pollution could alter the
urinary level of CC16.
References
1. Timonen KL, Hoek G, Heinrich J, et al. Daily variation in fine and
ultrafine particulate air pollution and urinary concentrations of lung
Clara cell protein CC16. Occup Environ Med 2004; 61:908-14.
2. Laing IA, Goldblatt J, Eber E, et al. A polymorphism of the CC16
gene is associated with an increased risk of asthma. J Med Genet 1998;
35:463-7.
3. Laing IA, Hermans C, Bernard A, et al. Association between plasma
CC16 levels, the A38G polymorphism, and asthma. Am J Respir Crit Care Med
2000; 161:124-7.
4. Sengler C, Heinzmann A, Jerkic SP, et al. Clara cell protein 16
(CC16) gene polymorphism influences the degree of airway responsiveness in
asthmatic children. J Allergy Clin Immunol 2003; 111:515-9.
5. Saadat M, Saadat I, Saboori Z, et al. Combination of CC16, GSTM1
and GSTT1 genetic polymorphisms is associated with asthma. J Allergy Clin
Immunol 2004; 113:996-8.
In a letter, Greenberg,[1] commenting on our paper,[2] raises a
number of points with which we disagree.
There is now a broad consensus that amphiboles are vastly more
dangerous than chrysotile in their propensity to produce mesothelioma, and
even a casual review of the literature indicates that where there is a
continuing increase in mesothelioma rates, it is seen in countries that
used la...
In a letter, Greenberg,[1] commenting on our paper,[2] raises a
number of points with which we disagree.
There is now a broad consensus that amphiboles are vastly more
dangerous than chrysotile in their propensity to produce mesothelioma, and
even a casual review of the literature indicates that where there is a
continuing increase in mesothelioma rates, it is seen in countries that
used large amounts of amosite and crocidolite, as we indicated in our
paper.
He raises the issue of whether asbestosis must be present to
attribute a lung cancer to asbestos exposure. Our paper was not about
this issue, we did not say anything about necessary sequence and the
phrase he cited was the lone mention of this issue, included in the
introduction before focusing on the main subject: mesothelioma. However,
since Greenberg raises the subject, the Wilkerson et al paper[3] was in no
way a "consensus" by a "group of experts", rather it was the report of a
study of hospitalized patients, a study which had a number of serious
flaws, as we explained in our published response.[4] Also, even if one
assumes that lung cancers can be generated by high exposure to asbestos
without the presence of asbestosis, it makes no sense to expect an
increased lung cancer risk in the face of declining asbestos usage and
increased control of exposure, exactly the factors that are driving the
decreased rates of mesothelioma. Greenberg’s own words clearly indicate
that he is more interested in the "adversarial spectrum" than the science!
Greenberg complains about the use of national import tonnage as an
indicator of potential overall worker exposures to the various asbestos
fiber types. There is no other way to do this, and this approach has been
used by Peto,[5] and in a previous publication of ours, comparing US and
UK mesothelioma trends.[6]
We don’t know exactly what paper Greenberg refers to in his comments
about events that occur in test tubes within 4 minutes, but in vitro
experimental data must always give way to in vivo experimental data, and
the latter to human epidemiology. Greenberg is actually incorrect in
stating that all types of fibers are equally potent causes of malignancies
in animals. In fact, proper analysis of the original Wagner inhalation
experiments in rats indicates that, because the asbestos was delivered on
an equal mass and not equal fiber number basis, the number of chrysotile
fibers to which the animals were exposed was vastly greater than the
number of amphibole fibers but the number of mesotheliomas found was about
the same, thus indicating the greater potency of amphiboles in causing
mesothelioma. This conclusion has been confirmed for both mesothelioma and
lung carcinoma in more modern animal inhalation studies, comprehensively
reviewed,[7] and there is in fact considerable evidence that lung cancers
in animals exposed to asbestos only develop when asbestosis is present.[8]
Greenberg raises a number of other issues, but the overall thrust of
his letter appears to be that declining rates of (readily apparent)
asbestos-induced disease should not be viewed as indicating a foreseeable
end to the asbestos problem. Yet if declining rates of disease don’t
indicate a problem that, with proper control of exposure, will slowly
disappear, what will?
Finally, Greenberg closes with kudos for a conference entitled The
Third Wave of Asbestos Disease.[9] In the view of most investigators in
this field, this conference contributed little to the knowledge base on
asbestos-related diseases and served mainly as a political/litigation
brief. One wonders if there will ever come a time when any good news
about asbestos-related health effects is welcomed by all who profess to
have worker health as their primary motivation.
References
(1) Greenberg M. Changing trends in US mesothelioma incidence. Occup
Environ Med 2005;62:133–134.
(2) Weill H, Hughes JM, Churg AM. Changing trends in US mesothelioma
incidence. Occup Environ Med. 2004 May;61(5):438-41.
(3) Wilkinson P, Hansell DM, Janssens S, et al. Is lung cancer
associated with asbestos exposure when there are no small opacities in the
chest
radiograph? Lancet 1995;345:1074–8.
(4) Weill H, Hughes JM, Jones RN. Asbestos: a risk too far? Lancet
1995; 346:304.
(5) Peto J, Hodgson JT, Matthews FE, Jones JR. Continuing increase in
mesothelioma mortality in Britain. Lancet. 1995 Mar 4;345(8949):535-9.
(6) Weill H, Hughes JM. Mesothelioma. Lancet 1995; 345:1234.
(7) Hesterberg TW, Hart GA: Synthetic vitreous fibers: a review of
toxicology research and its impact on hazard classification. Crit Rev
Toxicol 2001;31:1-53.
(8) Davis JM, Cowie HA. The relationship between fibrosis and cancer
in experimental animals exposed to asbestos and other fibers. Environ
Health Perspect 1990;88:305-309.
(9) The Third Wave of Asbestos Disease: Exposure to Asbestos in Place
--Public Health Control. Conference. New York, New York, June 7-9, 1990.
Ann N Y Acad Sci. 1991 Dec 31;643:1-625.
As Punnett correctly pointed out in her editorial,[1] we called attention to the need to determine the
causes of perceived muscular tension (PMT) in our paper.[2] Unfortunately, the
PMT data was only collected at the baseline of the study and not at any of
the 10 follow-ups. Due to the lack of longitudinal data we could not
explore the cause(s) of PMT in our analyses.
As Punnett correctly pointed out in her editorial,[1] we called attention to the need to determine the
causes of perceived muscular tension (PMT) in our paper.[2] Unfortunately, the
PMT data was only collected at the baseline of the study and not at any of
the 10 follow-ups. Due to the lack of longitudinal data we could not
explore the cause(s) of PMT in our analyses.
Punnett also raises the issue that any other occupational effects (in
this case physical and/or psychosocial exposure) are underestimated in the
analyses that are adjusted for PMT. This is a correct observation, though
we have presented both univariate and multivariate analyses in the paper
and the results in the univariate and the multivariate analyses do not
differ that much and the same patterns are observed in both analyses.
Following the above mentioned observations, Punnett
comments that the results provide less information than we might wish
to have regarding which interventions would decrease muscle tension and
resulting neck pain. Although the study did not reveal what factors
cause PMT, we believe that the results indicate that PMT can be used
both in health surveillance and in health screening. Work places where a high prevalence of PMT is found should be prioritized for interventions
(eg health surveillance). These interventions can target both
psychosocial and ergonomic work factors. In health screening, individuals
with high PMT can be targeted for further examination of possible job and
home psychosocial and ergonomic stressors.
Furthermore we suggest that interventions against high PMT conducted
by the occupational health services should focus on more than one risk
factor. For example, an intervention could comprise optimisation of the
workplace layout (modifying the physical demands) in combination with a
feedback survey of the psychosocial work environment (modifying the
psychosocial factors) and individual training focusing on working and
relaxation technique (modifying the individual factors). Although we do
not yet have support for this recommendation by data from RCTs of reducing
PMT there are interventions studies showing effects on discomfort by
multifactor ergonomic actions.[3]
References
1. Punnett L. Work related neck pain: how important is it, and how should we understand its causes? Occup Environ Med 2004; 61: 954-955.
2. Wahlström J, Hagberg M, Toomingas A et al. Perceived
muscular tension, job strain, physical exposure, and associations with
neck pain among VDU users; a prospective cohort study. Occup Environ Med 2004 61(6): 523-8.
3. Ketola R, Toivonen R, Häkkänen M et al. Effects of ergonomic
intervention in work with video display units. Scand J Work Environ Health 2002 28(1): 18-24.
Dear Editor,
Firstly, latent period always refers to the period between the point of the time when disease occurs and point of the time when the disease is detected, while tumour induction time refers to the period between the point of the time when the component cause (can be an exposure) is satisfied and the point of the time when the disease is occurred.[1] Thus only under the extreme condition that one secon...
Dear Editor,
The paper by Nicholson et al. provides useful evidence-based guidelines for prevention, identification, and management of occupational asthma (OA) based on a comprehensive review of the literature.[1]
Evidence statements 6 and 7 list the workers most commonly reported to OA surveillance schemes or reported from population studies to be at increased risk of developing asthma. Hairdressers are n...
Dear Editor,
The review of occupational asthma by Nicholson et al. [1] is comprehensive. It is an important report that is likely to be widely read: the evidence review of low back pain has, for example, been one of the most commonly downloaded articles [2]. The appearance in the principal recommendations of the authors’ unsubstantiated opinions is, therefore, concerning.
The authors also include issues...
Dear Editor,
Timonen and colleagues reported the association between urinary concentration of lung Clara cell protein CC16, a marker for lung damage, and daily variation in fine and ultrafine particulate air pollution in three cities of Netherlands (Amsterdam), Germany (Erfurt), and Finland (Helsinki). They found that in Amsterdam and Erfurt, there were no significant association between PM2.5 and concentration...
Dear Editor
In a letter, Greenberg,[1] commenting on our paper,[2] raises a number of points with which we disagree.
There is now a broad consensus that amphiboles are vastly more dangerous than chrysotile in their propensity to produce mesothelioma, and even a casual review of the literature indicates that where there is a continuing increase in mesothelioma rates, it is seen in countries that used la...
Dear Editor
As Punnett correctly pointed out in her editorial,[1] we called attention to the need to determine the causes of perceived muscular tension (PMT) in our paper.[2] Unfortunately, the PMT data was only collected at the baseline of the study and not at any of the 10 follow-ups. Due to the lack of longitudinal data we could not explore the cause(s) of PMT in our analyses.
Punnett also raises the i...
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